Equine Encephalitis Virus

Introduction

Family Togaviridae

Genus Alphavirus Single-stranded, linear, positive-sense RNA viruses, 60-70nm in diameter..</ref>

(Surface of an Alphavirus. This image is a computer-generated model of the surface of an alphavirus derived by cryoelectron microscopy. The spike-like structures on the virion surface are trimers composed of heterodimers of the virion surface glycoproteins E1 and E2. These spikes are used by the virus to attach to susceptible animal cells. Sourced from Wikimedia Commons, Copyright of the Centers for Disease Control and Prevention (CDC) Division of Vector-Borne Infectious Diseases, 2007)

Important Serotypes

Several alphavirus strains have been isolated during equine and human epidemics of encephalitis in the Western Hemisphere. These epidemics have most often been attributed to:

• Eastern Equine Encephalitis virus (EEV)
• Western EEV
• Venezuelan EEV.

Eastern EEV has North and South American antigenic variants. Western EEV is a recombinant between an Eastern EEV-like virus and a Sindbis-like virus. Western EEV also has two antigenic subtypes - WEE and Highlands J viruses. Considerable overlap exists between the various strains in terms of their geography, and potentially also in their antigenic properties and biological behaviour. Of the 6 subtypes of Venezuelan EEV (I-VI), significant outbreaks of equine encephalitis in the Western Hemisphere over the last two decades have been caused by IAB, IC and IE. Variant ID from Central America and variant IF from Brazil are considered endemic and typically demonstrate low pathogenicity for horses. These features are also typical of subtype II (Everglades) virus in Florida and types II, IV, V ad VI viruses.

Diseases

Arboviruses are the most common cause of equine encephalitis.

Distribution

Virus distribution is largely dictated by the distribution of appropriate vectors. Thus Eastern EEV can be found in a region extending from eastern Canada at its northern extremity, down throughout the Caribbean and in parts of Central and South America. The virus has also been identifed in the Philippines and may be present in Europe. Over the last two decades, Western EEV has rarely caused disease in the western United States, although it is found here in avian reservoir hosts. As well as producing disease outbreaks in Mexico, Venezuela and Colombia, Venezuelan EEV has recently been recognized in Peru, Brazil, French Guiana and Trinidad.

Reservoirs

Togaviridae survive by asymptomatically infecting sylvatic hosts such as birds, small mammals, reptiles and amphibians. Overwintering occurs in these wild populations.

Vectors

During a blood meal, mosquito vectors transmit viral particles between wild animal hosts. Viruses that are able to penetrate the mosquito's gut can pass via the haemolymph to the oral glands. Here, viral replication is followed by the shedding of viral particles into the saliva and other oral secretions. Viral multiplication may not be necessary for transmission if the original blood meal contained sufficient numbers of viral particles. It is thought that the mosquito remains permanently infected. The most significant disease vectors for each viral serotype are:

• Eastern EEV: Aedes spp.
• Western EEV: Culex tarsalis
• Venezuelan EEV: Culex melanconium, Aedes spp., Phosphora spp.

Culiseta melanura is another vector for Eastern EEV. It feeds mostly on swamp birds, completing an enzootic cycle of viral transmission. C.melanura is thus an inhabitant of freshwater swamps and is not usually found in areas densely populated by equids. Epizootics and epidemics of Eastern EEV disease are propagated by Aedes spp. Western EEV persists in an enzootic cycle with passerine birds, transmitted by C.tarsalis. Other vectors or overwintering hosts for this serotype may include Dermacentor andersoni ticks, Triatoma sanguisuga (the assassin bug), and the cliff swallow bug (Oeciacus vicarius). Epidemic strains of Venezuelan EEV have infected mosquito species from several genera and this viral serotype may also be transmitted by ticks.

Virus Identification

Viruses can be identified by complement fixation, immunofluorescence, PCR, ELISA, or virus isolation.

• The complement fixation test can be used to identify Eastern or Western EEV in infected mouse or chicken brains, cell culture fluid or amniotic-allantoic fluid
• Virus may be identified in brain tissue or cell culture using direct immunofluorescent staining.
• EEE and WEE viral RNA in mosquitoes and equine tissues may be detected by reverse-transcription PCR.
• ELISA can be used to detect virus in brain tissue. An antigen-capture ELISA, developed for EEE surveillance in mosquitoes, can be used where virus isolation and PCR facilities are unavailable.
• Virus isolation is the most definitive diagnostic method for EEE or WEE. Brain is preferred, but virus has also been isolated from the liver and spleen. Samples of these tissues should be taken in duplicate, one set for virus isolation and the other placed in formalin for histopathology. Viral isolation specimens should be sent frozen unless they can be received refrigerated within 48 hours of sampling. Unless clinical signs persist for more than 5days prior to death, EEE virus is frequently isolated from equine brain tissue. WEE virus, however, is rarely isolated from tissues of infected horses. Newborn mice, chicken embryos and a number of cell culture systems can be used for virus isolation. Virus may also be isolated from cerebrospinal fluid (CSF) of acutely infected horses.

References

Also known as:

EEV Alphavirus Eastern Equine Encephalitis Virus, EEE Western Equine Encephalitis Virus, WEE Venezuelan Equine Encephalitis Virus, VEE