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Information on Arboviral EncephalitidesPerspective PerspectiveArthropod-borne viruses, i.e. arboviruses, are viruses that are maintained in nature through biological transmission between susceptible vertebrate hosts by blood feeding arthropods (mosquitoes, psychodids, ceratopogonids, and ticks). Vertebrate infection occurs when the infected arthropod takes a blood meal. The term 'arbovirus' has no taxonomic significance. Arboviruses that cause human encephalitis are members of three virus families: the Togaviridae (genus Alphavirus), Flaviviridae, and Bunyaviridae. All arboviral encephalitides are zoonotic, being maintained in complex life cycles involving a nonhuman primary vertebrate host and a primary arthropod vector. These cycles usually remain undetected until humans encroach on a natural focus, or the virus escapes this focus via a secondary vector or vertebrate host as the result of some ecologic change. Humans and domestic animals can develop clinical illness but usually are "dead-end" hosts because they do not produce significant viremia, and do not contribute to the transmission cycle. Many arboviruses that cause encephalitis have a variety of different vertebrate hosts and some are transmitted by more than one vector. Maintenance of the viruses in nature may be facilitated by vertical transmission (e.g., the virus is transmitted from the female through the eggs to the offspring). Arboviral encephalitides have a global distribution, but there are four main virus agents of encephalitis in the United States: eastern equine encephalitis (EEE), western equine encephalitis (WEE), St. Louis encephalitis (SLE) and LaCrosse (LAC) encephalitis, all of which are transmitted by mosquitoes. Another virus, Powassan, is a minor cause of encephalitis in the northern United States, and is transmitted by ticks. A new Powassan-like virus has recently been isolated from deer ticks. Its relatedness to Powassan virus and its ability to cause disease has not been well documented. Most cases of arboviral encephalitis occur from June through September, when arthropods are most active. In milder (i.e., warmer) parts of the country, where arthropods are active late into the year, cases can occur into the winter months. The majority of human infections are asymptomatic or may result in a nonspecific flu-like syndrome. Onset may be insidious or sudden with fever, headache, myalgias, malaise and occasionally prostration. Infection may, however, lead to encephalitis, with a fatal outcome or permanent neurologic sequelae. Fortunately, only a small proportion of infected persons progress to frank encephalitis. Experimental studies have shown that invasion of the central nervous system (CNS), generally follows initial virus replication in various peripheral sites and a period of viremia. Viral transfer from the blood to the CNS through the olfactory tract has been suggested. Because the arboviral encephalitides are viral diseases, antibiotics are not effective for treatment and no effective antiviral drugs have yet been discovered. Treatment is supportive, attempting to deal with problems such as swelling of the brain, loss of the automatic breathing activity of the brain and other treatable complications like bacterial pneumonia. There are no commercially available human vaccines for these U.S.. diseases. There is a Japanese encephalitis vaccine available in the U.S. A tick-borne encephalitis vaccine is available in Europe. An equine vaccine is available for EEE, WEE and Venezuelan equine encephalitis (VEE). Arboviral encephalitis can be prevented in two major ways: personal protective measures and public health measures to reduce the population of infected mosquitoes. Personal measures include reducing time outdoors particularly in early evening hours, wearing long pants and long sleeved shirts and applying mosquito repellent to exposed skin areas. Public health measures often require spraying of insecticides to kill juvenile (larvae) and adult mosquitoes. Selection of mosquito control methods depends on what needs to be achieved; but, in most emergency situations, the preferred method to achieve maximum results over a wide area is aerial spraying. In many states aerial spraying may be available in certain locations as a means to control nuisance mosquitoes. Such resources can be redirected to areas of virus activity. When aerial spraying is not routinely used, such services are usually contracted for a given time period. Financing of aerial spraying costs during large outbreaks is usually provided by state emergency contingency funds. Federal funding of emergency spraying is rare and almost always requires a federal disaster declaration. Such disaster declarations usually occur when the vector-borne disease has the potential to infect large numbers of people, when a large population is at risk and when the area requiring treatment is extensive. Special large planes maintained by the United States Air Force can be called upon to deliver the insecticide(s) chosen for such emergencies. Federal disaster declarations have relied heavily on risk assessment by the CDC. Laboratory diagnosis of human arboviral encephalitis has changed greatly over the last few years. In the past, identification of antibody relied on four tests: hemaglutination-inhibition, complement fixation, plaque reduction neutralization test, and the indirect fluorescent antibody (IFA) test. Positive identification using these immunoglobulin M (IgM) - and IgG-based assays requires a four-fold increase in titer between acute and convalescent serum samples. With the advent of solid-phase antibody-binding assays, such as enzyme-linked immunosorbent assay (ELISA), the diagnostic algorithm for identification of viral activity has changed. Rapid serologic assays such as IgM-capture ELISA (MAC-ELISA) and IgG ELISA may now be employed soon after infection. Early in infection, IgM antibody is more specific, while later in infection, IgG antibody is more reactive. Inclusion of monoclonal antibodies (MAbs) with defined virus specificities in these solid phase assays has allowed for a level of standardization that was not previously possible. Virus isolation and identification have also been useful in defining viral agents in serum, cerebrospinal fluid and mosquito vectors. While virus isolation still depends upon growth of an unknown virus in cell culture or neonatal mice, virus identification has also been greatly facilitated by the availability of virus-specific MAbs for use in IFA assays. Similarly, MAbs with avidities sufficiently high to allow for specific binding to virus antigens in a complex protein mixture (e.g., mosquito pool suspensions) have enhanced our ability to rapidly identify virus agents in situ. While polymerase chain reaction (PCR) has been developed to identify a number of viral agents, such tests have not yet been validated for routine rapid identification in the clinical setting. Mosquito-borne encephalitis offers a rare opportunity in public health to detect the risk of a disease before it occurs and to intervene to reduce that risk substantially. The surveillance required to detect risk is being increasingly refined by the potential utilization of these new technologies which allows for rapid identification of dangerous viruses in mosquito populations. These rapid diagnostic techniques used in threat recognition can shorten public health response time and reduce the geographic spread of infected vectors and thereby the cost of containing them. The Arbovirus Diseases Branch of NCID's Division of Vector-Borne Infectious Diseases has responsibility for CDC's programs in surveillance, diagnosis, research and control of arboviral encephalitides. Eastern Equine EncephalitisEastern equine encephalitis (EEE) is also caused by a virus transmitted to humans and equines by the bite of an infected mosquito. EEE virus is an alphavirus that was first identified in the 1930's and currently occurs in focal locations along the eastern seaboard, the Gulf Coast and some inland Midwestern locations of the United States. While small outbreaks of human disease have occurred in the United States, equine epizootics can be a common occurrence during the summer and fall. It takes from 4-10 days after the bite of an infected mosquito for an individual to develop symptoms of EEE. These symptoms begin with a sudden onset of fever, general muscle pains, and a headache of increasing severity. Many individuals will progress to more severe symptoms such as seizures and coma. Approximately one-third of all people with clinical encephalitis caused by EEE will die from the disease and of those who recover, many will suffer permanent brain damage with many of those requiring permanent institutional care. In addition to humans, EEE virus can produce severe disease in: horses, some birds such as pheasants, quail, ostriches and emus, and even puppies. Because horses are outdoors and attract hordes of biting mosquitoes, they are at high risk of contracting EEE when the virus is present in mosquitoes. Human cases are usually preceded by those in horses and exceeded in numbers by horse cases which may be used as a surveillance tool. EEE virus occurs in natural cycles involving birds and Culiseta melanura, in some swampy areas nearly every year during the warm months. Where the virus resides or how it survives in the winter is unknown. It may be introduced by migratory birds in the spring or it may remain dormant in some yet undiscovered part of its life cycle. With the onset of spring, the virus reappears in the birds (native bird species do not seem to be affected by the virus) and mosquitoes of the swamp. In this usual cycle of transmission, virus does not escape from these areas because the mosquito involved prefers to feed upon birds and does not usually bite humans or other mammals. For reasons not fully understood, the virus may escape from enzootic foci in swamp areas in birds or bridge vectors such as Coquilletidia perturbans and Aedes sollicitans. These species feed on both birds and mammals and can transmit the virus to humans, horses, and other hosts. Other mosquito species such as Ae. vexans and Culex nigripalpus can also transmit EEE virus. When health officials maintain surveillance for EEE virus activity, this movement out of the swamp can be detected, and if the level of activity is sufficiently high, can recommend and undertake measures to reduce the risk to humans.
Centers for Disease Control and Prevention, National Center for Infectious Diseases, Division of Vector-Borne Infectious Diseases, 1300 Rampart Road, Colorado State University Foothills Research Campus, P.O. Box 2087, Fort Collins, Colorado 80522, USA; telephone: (970)221-6400; fax: (970)221-6476 Every effort has been made to provide correct, complete and up-to-date pest management information for New York State in this publication. Changes in pesticide regulations thus occur constantly, and human errors are still possible. These recommendations are not a substitute for pesticide labeling. Before using any product, chemical, or pesticide, read carefully, understand, and follow strictly any instructions on the product label. The above information has been obtained from sources believed to be reliable. None of the employees of Ocean-Beach.com have verified the correctness of any information contained herein.
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