Venezuelan Equine Encephalitis (VEE) Infection in Horses
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Abstract:
Venezuelan equine encephalitis (VEE) is caused by a virus in the family Togaviridae genus Alphavirus. It is an enveloped virus with an icosahedral capsid 60 to 70 nm in diameter with a linear, single-stranded positive-sense RNA nonsegmented genome of approximately 11.4 kilobases (4). VEE periodically occurs in South and Central America and occurred in Texas in 1971 (6). VEE viruses exist in two settings: (i) a continuous cycle maintained between Culex mosquito vectors and rodents (enzootic), and (ii) epidemics that involve several mosquito species that feed on mammals (epizootic). Epizootic VEE virus varients occur in irregular epizootic cycles and cause clinical disease and deaths in equines only during those cycles. Sylvatic or enzootic VEE viruses may be found at any time in enzootic cycles involving rodents; equine disease is rarely associated with infection by sylvatic VEE viruses. Aedes taeniorhynchus is thought to be the main mosquito vector (1); however, other mosquitoes are thought to play a role, and during an epidemic in horses in 1969 to 1971 Aedes aegypti, Culex tarsalis, Deinocerites pseudes, and Psorophora confinnis mosquitoes were shown to be infected. This epidemic began in 1969 in northern South America and by the time it ended in 1971, it had resulted in the deaths of hundreds of thousands of horses throughout Central America, Mexico, and Texas (3). Female mosquitoes ingest the virus when bloodfeeding on infected rodents or horses to obtain protein for egg production and after a 7 to 20 day extrinsic incubation period can transmit the virus when feeding on a new host. The mosquitoes remain infected for life. The principal mosquito vector for human infections is thought to be Culex pipiens although more than 30 other species have been implicated (5)
Usually 0.5 to 5 days after being bitten by an infected mosquito, horses begin to show signs. Infections range from asymptomatic, to mild (anorexia, fever), or severe either with fatality or without. Horses with a severe response show a distinctive lack of coordination that leads to a leaning stance and circling due to the swelling of the brain (Fig. 1–3). Other signs include fever, lack of appetite with rapid weight loss, and depression, and may include seizures. The sylvatic virus is endemic in northern South America, Trinidad, Central America, Mexico, and Florida. Epizootic virus appears sporadically in epizootics mostly in Mexico, Central and South America. The photos shown here were taken in Gualaca, Panama. Prognosis is poor for horses infected with epizootic viruses (50 to 90% mortality). Horses often die from trauma induced during seizures. Figure 4 shows a horse that has died, and shows lesions on the eyes and face incurred during seizures. Also note the lack of vegetation around the head, which is caused as the horse's head swings back and forth during the seizures. Similar defoliation is also often noted near the legs of horses that die of VEE as their legs will swing in a paddling motion. Upon necropsy the brain shows signs of encephalitis (swelling of the brain) and hemorrhaging that is actually caused by head trauma during the seizures rather than viral damage (Fig. 5). Horses are often euthanatized before they reach this point, as recovery in cases this severe is rare (3, 6). There is a vaccine to control this disease that should be administered yearly and also contains western and eastern encephalitis viruses along with VEE viruses.
Similar to western and eastern encephalitis, humans can become infected with VEE. In humans, signs of VEE infection include fever, exhaustion, back pain, nausea, vomiting, and headache; children are at greatest risk for developing central nervous system infections. The overall mortality rate in epidemics is 0.5 to 1%. In patients who develop encephalitis, the mortality rate is about 20%, in the absence of adequate medical care this can approach 25 to 30%. Encephalitis is clinically diagnosed in only 1 to 4% of adults and 3 to 5% of children. There is no vaccination for humans (3).
The virus is cultivated typically in
cell culture and quantified using plaque assays; virus is serially diluted and plated on the African green monkey kidney cell line Vero V76 cells and cytopathic effect is quantified. Diagnosis is usually attempted using paired serums (acute and convalescent; 2 weeks apart) assaying for a four-fold increase in serum neutralizing antibody titers. This assay detects antibodies in the serum, if animals have had an immune response. However, this is problematic as many animals die before the second, 2 week, convalescent sample can be obtained (6).
See also:
Venezuelan Equine Encephalitis Virus
References.
1. Brault, A. C., A. M. Powers, and S. C. Weaver. 2002. Vector infection determinants of Venezuelan equine encephalitis virus reside within the E2 envelope glycoprotein. J. Virol. 76
:6387–6392.
2. Committee on Foreign Animal Diseases of the United States Animal Health Association. 1998, revision date. The Gray book of foreign animal diseases, 6th ed. United States Animal Health Association, Richmond, Va. [Online.] http://www.vet.uga.edu/VPP/gray_book/FAD/index.htm.
3. Fenner, F., P. A. Bachmann, E. P. J. Gibbs, F. A. Murphy, M. J. Studdert, and D. O. White. 1987. Veterinary virology, p. 460–462. Academic Press, Inc., Orlando, Fla.
4. Griffin, D. E. 2001. Alphaviruses, p. 917–962. In D. M. Knipe and P. M. Howley (ed.), Fields virology. Lippincott Williams and Wilkins, Philadelphia, Pa.
5. Nasci, R. S., and B. R. Miller. Culicine mosquitoes and the agents they transmit, p. 85–97. In B. J. Beaty and W. C. Marquardt (ed.), The biology of disease vectors. University Press of Colorado, Niwot, Colo.
6. Roberts, W. A., and G. A. Carter. 1976. Essentials of veterinary virology, p. 107. Michigan State University Press, East Lansing, Mich.Keywords:
Enzootic
Epizootic
Togaviridae
Alphavirus infection
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West Nile (WN) virus was identified in the Western Hemisphere in 1999. Along with human encephalitis cases, 20 equine cases of WN virus were detected in 1999 and 23 equine cases in 2000 in New York. During both years, the equine cases occurred after human cases in New York had been identified.
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Venezuelan equine encephalitis virus (VEEV) is an emerging pathogen of equids and humans, but infection of its rodent reservoir hosts has received little study. To determine whether responses to infection vary among geographic populations, we inoculated 3 populations of cotton rats with 2 enzootic VEEV strains (Co97-0054 [enzootic ID subtype] and 68U201 [enzootic IE subtype]). The 3 populations were offspring from wild-caught cotton rats collected in a VEE-enzootic area of south Florida, USA; wild-caught cotton rats from a non-VEE-enzootic area of Texas, USA; and commercially available (Harlan) colony-reared cotton rats from a non-VEE-enzootic region. Although each population had similar early viremia titers, no detectable disease developed in the VEE-sympatric Florida animals, but severe disease and death affected the Texas and Harlan animals. Our findings suggest that the geographic origins of cotton rats are important determinants of the outcome of VEE infection and reservoir potential of these rodents.
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SummaryAedes sollicitans mosquitoes became infected with Eastern equine encephalitis (EEE) from feeding upon an inoculated horse. These mosquitoes, after two weeks' incubation, transmitted infection by bite to a normal horse. Attempts to infect more mosquitoes by permitting them to feed upon this second horse met with failure. The virus which circulated in the blood of the inoculated horse titered as high as 10-5.5, a level not commonly attained in horses. The horse infected by mosquito bite had a lower, more usual concentration of virus in its blood, inadequate to infect mosquitoes. The results of these studies prove it possible for an occasional horse to serve as an EEE infection source for mosquitoes. It is believed, however, that horses rarely play an important role in EEE propagation.
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We determined whether mosquitoes infected with the viruses St. Louis encephalitis (SLE) or Venezuelan equine encephalitis inoculate virus extravascularly or directly into the vascular system. Infected mosquitoes fed on the distal 3rd of the tails of suckling mice. Significantly more mice whose tails were amputated at the midpoint within 10 min of mosquito feeding survived than did siblings whose tails remained intact. Even when tails were amputated 1–6 h after SLE virus-infected mosquitoes fed, the median time to death was significantly longer in mice with amputated tails (7.1 d) than in mice with intact tails (5.8 d). We concluded that mosquitoes inoculated virus primarily extravascularly, rather than directly into the vascular system, while feeding on a vertebrate host. Extravascular, rather than intravascular, delivery of pathogens by mosquitoes may affect disease pathogenesis and vaccine efficacy.
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A study was undertaken to investigate an increase in reported cases of clinical encephalitis due to eastern equine encephalitis (EEE) virus in horses and to determine the natural vertebrate hosts of that virus. Horses, birds, and small mammals were sampled at sites in a contiguous area in St. Joseph and Kalamazoo counties, Michigan, from 25 August to 5 September 1980. Serum samples from four horses acutely ill with encephalitis and 16 of 39 pasture mates of ill horses had neutralizing (N) antibody against EEE virus (46.5%); no viruses were isolated from these 43 sera. None of 24 draft horses from a site in St. Joseph County 12 km southeast of the affected sites had EEE antibody. A strain of Cache Valley virus was isolated from the blood of one of the 24 draft horses. No viruses were isolated, and no antibodies to EEE virus were detected in 28 blood samples from small mammals captured at sites where equine cases of encephalitis were occurring. Six strains of EEE virus, five of Highlands J virus, and one of Flanders virus were isolated from the blood of 401 wild birds belonging to 42 species captured at eight sites in both counties. A total of 29.9% of the wild birds had EEE antibody. Five species of domestic birds, mostly chickens and ring-necked pheasants, were sampled in both counties. Six strains of EEE virus were isolated from 152 ring-necked pheasants; these included three isolates from the brains of dead birds. About 13% of 51 pheasants tested from two small flocks in backyard pens in Kalamazoo County and 9% of 103 pheasants tested from a large game farm in St. Joseph County had antibody to EEE virus. The source of the EEE virus and the factors responsible for this epizootic are unknown; however, the epizootic probably represented an explosive expansion of an enzootic level of virus transmission.
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Serial survey on the ecology of Japanese encephalitis (JE) virus was made in 1966 and 1967. In spring in the both years, wild caught females of Culex tritaeniorhynchus and many other species including a great number of hibernated females were examined for JE virus. In 1967, besides the above, wild caught females in spring were forced to engorge blood from susceptible pigs, and some days after, the engorged ones were examined for the virus and the pigs for HI antibody. However, no virus was found in all the mosquitoes examined, and no antibody was detected in the pigs. Nevertheless, in mid-spring in 1967 2-ME sensitive antibody was found in a few of slaughtered pigs. This facts is very important and it seems necessary to set forward the program of investigations. Japanese commonsnakes of six species were examined for the reservoir of JE virus in nature, but it was concluded that snakes play minor role as a natural source of the virus transmission even in the epidemic season. Despite of the fact that the starting time of epizootic in pigs and of the occurrence of infected mosquitoes was nearly the same in 1966 and 1967, the duration and size of the infection in mosquitoes and of the epidemic in men were shorter and smaller in 1967 than in the previous year. The reason seems that the larger number of infected mosquitoes at the starting time in late June,1967 caused ・ ・- ・ ■■ ■ Thiswork was supportedinpart byResearch GrantCCOO20sfrom Public Health Service, NationalcommunicableDiseasecenter,Atlanta,Georgla,U.S.A. ContributionNo・S27fromtheInstitutefor TropICalMedicine,NagasakilJniversityandNo. 175fromtheDepartmentofMedicalZoology,NagasakiUniversitySchoolofMedicine EcologicalStudies onJapanese Encephalitis Virus 1拍 earlier and more rapid rise in the HI antibody possessing rate of pigs at the early days of epizootic in them reducing the remaining rate of susceptible pigs as faster as about a half-month than in 1966, and this, in turn, caused subsequent infections in mosquitoes and then in men to be shorter in duration and smaller in size.
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Abstract A total of 12 horses of different breeds and ages were infected with West Nile virus (WNV) via the bites of infected Aedes albopictus mosquitoes. Half the horses were infected with a viral isolate from the brain of a horse (BC787), and half were infected with an isolate from crow brain (NY99-6625); both were NY99 isolates. Postinfection, uninfected female Ae. albopictus fed on eight of the infected horses. In the first trial, Nt antibody titers reached >1:320, 1:20, 1:160, and 1:80 for horses 1 to 4, respectively. In the second trial, the seven horses with subclinical infections developed Nt antibody titers >1:10 between days 7 and 11 post infection. The highest viremia level in horses fed upon by the recipient mosquitoes was approximately 460 Vero cell PFU/mL. All mosquitoes that fed upon viremic horses were negative for the virus. Horses infected with the NY99 strain of WNV develop low viremia levels of short duration; therefore, infected horses are unlikely to serve as important amplifying hosts for WNV in nature.
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Abstract : The recent introduction of Aedes albopictus into the Americas has led to concern that this mosquito might serve as a vector of both native as well as exotic viruses. Experimental and field data indicate that this species is capable of transmitting chikungunya, Japanese encephalitis, yellow fever, West Nile, Ross River, and all 4 serotypes of dengue viruses, as well as St. Louis encephalitis and western equine encephalitis viruses. We evaluated the potential of the F3 generation of a Houston, Texas strain of Ae. albopictus to transmit Rift Valley fever (RVF) virus. Female mosquitoes, 5 to 10 days old reared at 26 C with a 16:8 L:D photoperiod, were allowed to feed on an anesthetized hamster that had been inoculated with RVF virus 24 hours previously. Recovery of virus from the body, but not the legs, indicated that viral infection was limited to the midgut and had not disseminated to the hemocoel, while recovery of virus from both legs and body indicated that the mosquito had a disseminated infection. Ae. albopictus should be considered a potential vector of RVR virus, should it be introduced into the southern United States. Reprints.
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Evidence was sought during 1970–1975 of persistence of equine-virulent Venezuelan encephalitis (VE) virus in regions of Central America that were heavily involved in the epidemic-equine epizootic of 1969. (a) Four sentinel horses were exposed in an arid, upland region of the Atlantic drainage of Guatemala during August–October 1970, but no horse became infected, (b) The epicenter region of the 1969 outbreak, in southeastern Guatemala and southwestern El Salvador, was studied during July 1970–February 1974; no antibody developed in sentinel horses, sentinel hamsters did not die, mosquitoes yielded no virus, wild rats had no detectable VE virus HI antibody. Unexplained decreases in populations of wild terrestrial mammals possibly limited maintenance of VE virus. However, mosquitoes were plentiful and present in the same species composition found at a focus of enzootic VE virus about 35 km northwest of the epicenter region, (c) In studies at two Guatemalan ranches near the epicenter, where horses died in 1969, VE virus infected sentinel horses along one of three lakes on one ranch during the wet season of 1972 but not during the dry or wet seasons of 1973; the titers of neutralizing antibodies in these four horses were higher against an enzootic strain of VE virus than against an epizootic strain. During 1970 and 1971, VE virus was isolated from sentinel hamsters exposed at a marsh on the other ranch, but Vero plaque characteristics were those of enzootic VE virus, (d) The only epizootic activity of VE virus discovered in Central America in 1970–1975 occurred in Nicaragua between April and June 1972. Several hundred horses died, and N antibody, like that engendered by epizootic virus, was found in two young, unvaccinated horses. Whether this represented persistence of epizootic VE virus or reintroduction of virus is unknown.
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Journal Article EPIDEMIC VENEZUELAN EQUINE ENCEPHALITIS IN NORTH AMERICA IN 1971: VERTEBRATE FIELD STUDIES Get access W. D. SUDIA, W. D. SUDIA Address for reprint requests which should be addressed to W. D. Sudia Search for other works by this author on: Oxford Academic PubMed Google Scholar R. G. McLEAN, R. G. McLEAN Search for other works by this author on: Oxford Academic PubMed Google Scholar V. F. NEWHOUSE, V. F. NEWHOUSE Search for other works by this author on: Oxford Academic PubMed Google Scholar J. G. JOHNSTON, JR., J. G. JOHNSTON, JR. Search for other works by this author on: Oxford Academic PubMed Google Scholar D. L. MILLER, D. L. MILLER Search for other works by this author on: Oxford Academic PubMed Google Scholar H. TREVINO, H. TREVINO Search for other works by this author on: Oxford Academic PubMed Google Scholar G. S. BOWEN, G. S. BOWEN Search for other works by this author on: Oxford Academic PubMed Google Scholar G. SATHER G. SATHER Search for other works by this author on: Oxford Academic PubMed Google Scholar American Journal of Epidemiology, Volume 101, Issue 1, January 1975, Pages 36–50, https://doi.org/10.1093/oxfordjournals.aje.a112069 Published: 01 January 1975 Article history Received: 04 March 1974 Revision received: 26 August 1974 Published: 01 January 1975
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