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Topic:Eastern Equine Encephalitis

Eastern Equine Encephalitis (EEE) is a viral disease affecting horses, caused by the Eastern Equine Encephalitis virus, which is transmitted through mosquito bites. The virus primarily affects the central nervous system, leading to symptoms such as fever, depression, and neurological disturbances in infected horses. EEE is considered a significant health concern in equine populations due to its high mortality rate. Diagnosis is typically based on clinical signs, serological testing, and post-mortem examination. This page compiles peer-reviewed research studies and scholarly articles exploring the epidemiology, pathogenesis, clinical manifestations, and preventive measures related to Eastern Equine Encephalitis in horses.
Infection of a poikilothermic cell line (XL-2) with eastern equine encephalitis and western equine encephalitis viruses.
Journal of medical virology    March 1, 1987   Volume 21, Issue 3 277-281 doi: 10.1002/jmv.1890210311
Morier L, Cantelar N, Soler M.Eastern Equine Encephalitis (EEE) was in Cuba before the 1940s; the virus has been isolated from horses, birds, and rodents during epizootic as well as interepizootic periods. The only isolation of Western Equine Encephalitis (WEE) virus was from a sick pigeon found in the vicinity of Havana University. Both viruses can cause human disease; the isolation of WEE virus from the centre of an urban area emphasises the need for the prompt isolation and rapid identification of these agents. The object of this work was to compare the sensitivity of a continuous cell line (XL-2) from the toad, Xenopus...
Study of homologous and heterologous antibody response in California horses vaccinated with attenuated Venezuelan equine encephalomyelitis vaccine (strain TC-83).
American journal of veterinary research    March 1, 1978   Volume 39, Issue 3 371-376 
Ferguson JA, Reeves WC, Milby MM, Hardy JL.Of 359 horses vaccinated with attenuated Venezuelan equine encephalomyelitis (VEE) vaccine (strain TC-83), 87% developed hemagglutination-inhibition (HI) antibodies to VEE virus within 1 month. Blood from a subsample of 101 of the 359 horses was obtained over a 1-year period. Within 1 month after vaccination, 84% of the 101 horses had developed VEE HI antibodies, 87% had developed VEE-neutralizing (Nt) antibodies, and 78% had developed VEE complement-fixing (CF) antibodies. One year after vaccination, 58% of the horses had VEE HI antibodies and 73% had VEE Nt antibodies. The percentage of hors...
Eastern equine encephalitis in Massachusetts, 1957-1976. A prospective study centered upon analyses of mosquitoes.
American journal of epidemiology    February 1, 1978   Volume 107, Issue 2 170-178 doi: 10.1093/oxfordjournals.aje.a112519
Grady GF, Maxfield HK, Hildreth SW, Timperi RJ, Gilfillan RF, Rosenau BJ, Francy DB, Calisher CH, Marcus LC, Madoff MA.Reappearance of eastern equine encephalitis (EEE) in Massachusetts residents in the 1970's provided an opportunity to assess the predictive value of data on rainfall, EEE in horses, and carriage of EEE virus (EEEV) by mosquitoes, factors which had been studied annually since the last EEE outbreak in 1955-1956. The cycle of multiple cases during 1973-1975 started in a second consecutive year of rainfall that exceeded the annual mean by more than 20 cm, conditions recapitulating the 1955-1956 experience. In 1973, widespread EEE fatalities in horses presaged human cases, another recapitulation of...
[A comparative study of various genetic markers of eastern equine encephalomyelitis virus and its mutants induced by nitrous acid].
Voprosy virusologii    November 1, 1967   Volume 12, Issue 6 683-688 
Kitsak VIa, Fomina AN.No abstract available
Climatological Conditions Associated with Outbreaks of Eastern Equine Encephalitis.
The American journal of tropical medicine and hygiene    November 1, 1964   Volume 13 851-858 doi: 10.4269/ajtmh.1964.13.851
HAYES RO, HESS AD.No abstract available
An evaluation of various tissues in culture for isolation of eastern equine encephalitis virus.
Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)    January 1, 1958   Volume 97, Issue 1 152-158 doi: 10.3181/00379727-97-23673
MEDEARIS DN, KIBRICK S.No abstract available
Application of the paper disc technique to the collection of whole blood and serum samples in studies on eastern equine encephalomyelitis.
The Journal of infectious diseases    November 1, 1957   Volume 101, Issue 3 295-299 doi: 10.1093/infdis/101.3.295
KARSTAD L, SPALATIN J, HANSON RP.No abstract available
Equine encephalitis in Massachusetts.
The New England journal of medicine    October 10, 1957   Volume 257, Issue 15 701-704 doi: 10.1056/NEJM195710102571504
FEEMSTER RF.This research focuses on the first recognized human infection of equine encephalomyelitis, a disease mostly found in horses, which occurred in Massachusetts in the summer of 1938. The study dives […]
Eastern equine encephalomyelitis in Massachusetts; report of two cases, diagnosed serologically, with complete clinical recovery.
The New England journal of medicine    August 9, 1956   Volume 255, Issue 6 267-270 doi: 10.1056/NEJM195608092550604
DE WEBSTER HF.No abstract available
Eastern equine encephalitis in Connecticut: a serological survey of pheasant farmers.
The Yale journal of biology and medicine    February 1, 1955   Volume 27, Issue 4 287-296 
LIAO SJ.No abstract available
The sequelae of eastern equine encephalomyelitis.
The New England journal of medicine    June 16, 1949   Volume 240, Issue 24 960-962 doi: 10.1056/NEJM194906162402403
AYRES JC, FEEMSTER RF.No abstract available
Infectious equine encephalomyelitis in the United States in 1944.
The North American veterinarian    July 1, 1945   Volume 26 392-394 
MILLER AW.No abstract available
Studies on Eastern Equine Encephalomyelitis: III. Intraocular Infection with Fixed Virus in the Guinea Pig.
The Journal of experimental medicine    April 30, 1939   Volume 69, Issue 5 691-704 doi: 10.1084/jem.69.5.691
King LS.The behavior of a fixed strain of Eastern equine encephalomyelitis virus was studied in guinea pigs after intraocular inoculation. Such inoculation concerns the central and not the peripheral nervous system. The susceptibility to intraocular injection lies midway between the highly virulent intracerebral and the quite avirulent peripheral routes. The virus must act for 10 to 13 hours in order to induce a fatal infection. Removal of the inoculated eyeball before this interval almost always prevents fatality although it may allow immunity to develop. The virus, at suitable intervals after inject...