Arthropod-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. For more information :http://www.cdc.gov/ncidod/dvbid/Arbor/index.htm
La Crosse (LAC) encephalitis was discovered in La Crosse, Wisconsin in 1963. Since then, the virus has been identified in several Midwestern and Mid-Atlantic states. During an average year, about 75 cases of LAC encephalitis are reported to the CDC. Most cases of LAC encephalitis occur in children under 16 years of age. LAC virus is a Bunyavirus and is a zoonotic pathogen cycled between the daytime-biting tree hole mosquito, Ochlerotatus triseriatus, and vertebrate amplifier hosts (chipmunks, tree squirrels) in deciduous forest habitats. The virus is maintained over the winter by transovarial transmission in mosquito eggs. If the female mosquito is infected, she may lay eggs that carry the virus, and the adults coming from those eggs may be able to transmit the virus to chipmunks and to humans. For more information: http://www.cdc.gov/ncidod/dvbid/Arbor/lacfact.htm
Eastern 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 and require permanent institutional care. For more information : http://www.cdc.gov/ncidod/dvbid/Arbor/eeefact.htm
The alphavirus western equine encephalitis (WEE) was first isolated in California in 1930 from the brain of a horse with encephalitis, and remains an important cause of encephalitis in horses and humans in North America, mainly in western parts of the USA and Canada. In the western United States, the enzootic cycle of WEE involves passerine birds, in which the infection is inapparent, and culicine mosquitoes, principally Cx. tarsalis, a species that is associated with irrigated agriculture and stream drainages. The virus has also been isolated from a variety of mammal species. Other important mosquito vector species include Ochlerotatus melanimon in California, Oc. dorsalis in Utah and New Mexico and Oc. campestris in New Mexico. WEE virus was isolated from field collected larvae of Oc. dorsalis, providing evidence that vertical transmission may play an important role in the maintenance cycle of an alphavirus. For more information : http://www.cdc.gov/ncidod/dvbid/Arbor/weefact.htm
In the United States, the leading cause of epidemic flaviviral encephalitis is St. Louis encephalitis (SLE) virus. SLE is the most common mosquito-transmitted human pathogen in the U.S. While periodic SLE epidemics have occurred only in the Midwest and southeast, SLE virus is distributed throughout the lower 48 states. Since 1964, there have been 4,437 confirmed cases of SLE with an average of 193 cases per year (range 4 - 1,967). However, less than 1% of SLE viral infections are clinically apparent and the vast majority of infections remain undiagnosed. Illness ranges in severity from a simple febrile headache to meningoencephalitis, with an overall case-fatality ratio of 5-15 %. The disease is generally milder in children than in adults, but in those children who do have disease, there is a high rate of encephalitis. The elderly are at highest risk for severe disease and death. During the summer season, SLE virus is maintained in a mosquito-bird-mosquito cycle, with periodic amplification by peridomestic birds and Culex mosquitoes. In Florida, the principal vector is Cx. nigripalpus, in the Midwest, Cx. pipiens pipiens and Cx. p. quinquefasciatus and in the western United States, Cx. tarsalis and members of the Cx. pipiens complex. For more information : http://www.cdc.gov/ncidod/dvbid/sle/index.html
WNV is a flavivirus belonging
taxonomically to the Japanese encephalitis serocomplex that includes
the closely related St. Louis encephalitis (SLE) virus, Kunjin and
Murray Valley encephalitis viruses, as well as others. Since
West Nile virus (WNV) was first isolated in 1937, it has been known
to cause asymptomatic infection and fevers in humans in Africa, West
Asia, and the Middle East. Human and animal infections were not documented
in the Western Hemisphere until 1999. In 1999 and 2000, outbreaks
of WNV encephalitis (inflammation of the brain) were reported in persons
living in the New York City metropolitan area, New Jersey, and Connecticut.
In these two years, 83 human cases of West Nile illness were reported;
9 died. In 2001, human infection with WNV occurred in 10 states with
66 cases and 9 deaths. In 2002, WNV activity spread to 44 states,
with 4,156 human cases and 284 deaths. In
2003 there were 9,306 human cases in 45 states, with 240 deaths. In
2004 there were 2470 human cases in 41 states, with 88 deaths (Florida
had 41 human cases and 2 deaths). The majority of the cases occurred
in the western part of the U.S., particularly California (771 human
cases , 23 deaths) and Arizona (391 human cases , 14 deaths).
The disease is caused by the RVF virus, a member of the genus Phlebovirus in the family Bunyaviridae. The disease was first reported among livestock by veterinary officers in Kenya in the early 1900s.
Where is the disease
RVF virus primarily affects livestock and can cause disease in a large number of domestic animals (this situation is referred to as an "epizootic"). The presence of an RVF epizootic can lead to an epidemic among humans who are exposed to diseased animals. The most notable epizootic of RVF, which occurred in Kenya in 1950-1951, resulted in the death of an estimated 100,000 sheep. In 1977, the virus was detected in Egypt (probably exported there in infected domestic animals from Sudan) and caused a large outbreak of RVF among animals and humans. The first epidemic of RVF in West Africa was reported in 1987 and was linked to construction of the Senegal River Project. The project caused flooding in the lower Senegal River area and altered interactions between animals and humans resulting in transmission of the RVF virus to humans. For more visit http://www.cdc.gov/ncidod/dvrd/spb/mnpages/dispages/Fact_Sheets/Rift%20Valley%20Fever%20Fact%20Sheet.pdf
In Africa the virus is transmitted in three geographic regions: