- Eastern Equine
- Encephalomyelits
- Venezuelan Equine
- Encephalomyelits
- Wester Equine
- Encephalomyelitis
Species affected
Euryxen: Horse, Donkey, Mule, Rodents, Birds,
Humans —> Zoonotic!
- Eastern Equine
- Encephalomyelits
- Venezuelan Equine
- Encephalomyelits
- Wester Equine
- Encephalomyelitis
Most susceptible
All age groups
- Eastern Equine
- Encephalomyelits
- Venezuelan Equine
- Encephalomyelits
- Wester Equine
- Encephalomyelitis
Occurrence
Eastern: Canada, East coast of USA, Central America Western: Canada, West coast of USA, Mexico,
South America
Venezuelan: Southern states of USA, Central
and South America
Rarely in other continents
(detected in rodents and birds, without disease)
- Eastern Equine
- Encephalomyelits
- Venezuelan Equine
- Encephalomyelits
- Wester Equine
- Encephalomyelitis
Spread
*Eastern:
• Bird-Mosquito Cycle
• In mosquitos that have bird affinity
• Long lasting viraemia in birds
• Long-distance transmission (due to migratory birds)
• Seasonal and regional epidemics (mosquitos): Mainly in wetlands in summer
• Horse, turkey, pheasant, quail, ducks and humans > dead end hosts —> they do not shed the virus further
*Western:
• Bird-Mosquito-Rodent Cycle
• Appearance of disease depends on affinity of mosquitoes (birds vs mammals)
• Horse and humans are dead end hosts
*Venezuelan:
• Horse-Mosquito-Horse Cycle
• Prevalent in summer and rainy season (mosquitoes)
• Humans and horses are
not dead end hosts —> can shed the virus and spread the disease
- Eastern Equine
- Encephalomyelits
- Venezuelan Equine
- Encephalomyelits
- Wester Equine
- Encephalomyelitis
Pathogenesis
*Mosquito bite —> Regional lymph nodes —> First viraemia —>visceral organs —> Second viraemia (2-5 days) —> onset of clinical signs and infection of CNS
• Due to secondary viraemia occurring —> biphasic fever
*Course of disease is age and dose dependent
• Abortive infection: only the first fever seen
• Inapparent infection: no fever, low titre viraemia
*Convalescent animals have a lifelong immunity with partial cross-protection —> meaning that if recovered from EEE, can still be infected with WEE but clinical disease will be much less severe
- Eastern Equine
- Encephalomyelits
- Venezuelan Equine
- Encephalomyelits
- Wester Equine
- Encephalomyelitis
Primary replication
- Regional lymph nodes of bite wound
* Incubation period of 1-3 weeks
- Eastern Equine
- Encephalomyelits
- Venezuelan Equine
- Encephalomyelits
- Wester Equine
- Encephalomyelitis
Target organs
CNS
Muscles
- Eastern Equine
- Encephalomyelits
- Venezuelan Equine
- Encephalomyelits
- Wester Equine
- Encephalomyelitis
Clinical signs
*Peracute form:
• Fever (above 41℃), Shock
• Death within 12 hours
*Acute, Subacute form:
• Biphasic fever
• In the beginning: excitement and increased sensitivity
• Later: apathy, loss appetite, icterus
• Signs of encephalitis: visual disturbances,
head convulsions. paralysis
• Signs of myelitis: lameness, convulsions, paralysis
• Terminal stage —> death
• VEE: colic and diarrhoea too
*Chronic form:
• Rare
• Lasts 1-2 weeks
*Recovery is possible but with permanent damages
*Mortality varies:
• EEE: 78-98%
• WEE: 10-50%
• VEE: 32-86%
*Humans:
• Most often infected with VEEV
• Occurs simultaneously with outbreaks in horses (same vectors infect humans)
• Infection of pregnant women during 2nd-3rd trimester —> abortion, cerebral necrosis of newborn
• Children are more sensitive, more frequent CNS symptoms
• Fever, headache, nausea, vomiting, oedema of head and legs, cyanosis, convulsions, paralysis
• High mortality
• If recovery —> permanent defects
• Extensive epidemics in Central and South America
• Human vaccine available
- Eastern Equine
- Encephalomyelits
- Venezuelan Equine
- Encephalomyelits
- Wester Equine
- Encephalomyelitis
Pathology/histopathology
- Macroscopically not specific (eg icterus) —> cannot say it is Equine Encephalitis from pathology, check histopathology
- Encephalitis and myelitis affecting both grey and white matter —> presence of lymphatic cells and neutrophil granulocytes
- Blood vessel endothelial damage, thrombosis
- Chronic: degenerative and reparative processes
- Eastern Equine
- Encephalomyelits
- Venezuelan Equine
- Encephalomyelits
- Wester Equine
- Encephalomyelitis
Diagnosis
Clinical signs, seasonality and geographical origin —>
suspicion of disease but further testing required since disease is notifiable
Virus isolation on suckling
mouse brain, embryonate egg, cell cultures
RT-PCR, IHC
Serology: HAI, VN, CF
- Eastern Equine
- Encephalomyelits
- Venezuelan Equine
- Encephalomyelits
- Wester Equine
- Encephalomyelitis
Treatment
In enzootic countries (America):
• Supportive treatment
- Eastern Equine
- Encephalomyelits
- Venezuelan Equine
- Encephalomyelits
- Wester Equine
- Encephalomyelitis
Prevention and immunity
*In enzootic countries (America):
• Immunisation:
• Inactivated, trivalent vaccine containing all 3 viruses
• 2x basic immunisation and yearly boosters
• VEE: Attenuated strain T83
• To block an outbreak
• Mild residual virulence, transmission to escorts
• Vector control: proper drainage systems, insect repellants etc
*In EEEV / WEEV/ VEEV free countries:
• Avoid introduction of infected animals
• Repeated serological
investigations during quarantine
General Characteristics of Togavirus
- +ssRNA virus with an icosahedral capsule and an envelope
- Weak resistance in environnent (as enveloped) —> susceptible to heat, pH, dying out and detergents
- Antigenic diversity —> cross reactions die to having common antigens, some cross protection
- Arbovirus —> Mosquitos are vectors
- Genuses: Alphavirus (31 species), Rubivirus (1 species)
