presentation on viral encephalomyelitis of equine

2. Introduction
• Encephalomyelitis is the inflammation of the brain and spinal cord.
• Equine viral encephalomyelitis is an infectious mosquito-borne disease of horses, characterised
clinically by paralysis and other signs of nervous derangement.
• The virus can cause serious human disease as well as infecting poultry and other farmed birds
including quails, ostriches and emus.
• Equine viral encephalomyelitis is a disease which can be caused by several viruses (known as
equine encephalitis viruses). They include, but are not limited to:
i. Epidemic Venezuelan equine encephalomyelitis (VEE)
ii. Western equine encephalomyelitis (WEE)
iii. Eastern equine encephalomyelitis (EEE)
iv. Japanese encephalitis
v. West Nile virus
• Equine viral encephalomyelitis can be fatal, although some animals will recover from the disease.

3. Head pressing in horse Estern Equine Encephalitis

4. Etiology
• They are caused by alphaviruses from the Togaviridae family and are
serious zoonoses
• Alphaviruses are arthropod-borne members of the family Togaviridae.
They are small, enveloped viruses containing a single strand of
positive-sense RNA that comprise serologically differentiated
complexes.
• The enveloped virions are spherical, 60 to 70 nm in diameter & virions
mature by budding through the plasma membrane

5. Species Affected
• Equine viral encephalomyelitis mainly affects members of the equid family, such as:
i. horses
ii. donkeys
iii. mules
iv. zebras
• Other animals can also be affected, such as:
i. cattle, sheep and goats
ii. pigs
iii. birds, including poultry
iv. dogs
v. rodents
• Humans can also be affected

6. Epidemiology
• The three viruses are found in North, Central and South America,
with western equine encephalomyelitis being the most widely
distributed — from south-west Canada to most of South America
east of the Andes.
• Eastern equine encephalitis is found primarily in eastern Canada, US
states east of the Mississippi river, and the Caribbean islands.
• Western equine encephalitis is found in western Canada, US states
west of the Mississippi river, Mexico, and South America.
• Venezuelan equine encephalitis is found in Mexico, and Central and
South America.

7. Mode of Transmission
• Mosquitoes (Cluiseta melanura, Aedes vexans, Culiseta tarsalis,
Cluuicoides spp, Culex spp.)are responsible for transmitting all three
viruses.
• The natural cycle for EEE and WEE viruses is between birds and/or
small mammals and mosquitoes. Small outbreaks or sporadic cases
occur in humans and horses, which are generally regarded as ‘dead
end’ hosts. With VEE, the natural cycle is poorly understood, but is
believed to involve culicine mosquitoes and forest rodents.
• Epidemics in horses and humans occur at irregular intervals. There is a
high viraemia in horses and direct horse-mosquito cycles occur during
epidemics. The migratory birds should be considered as a factor of
spread of the disease.

8. Transmission of Virus in Animal

9. Clinical Signs
• The incubation of the disease after infection with the virus is from one to
three weeks
• In horses, EEE and WEE are indistinguishable clinically. Sub-clinical
infections can occur with both viruses. There is biphasic fever with clinical
signs appearing during the second peak. Affected horses show:
i. Hypersensitivity to sound and touch
ii. Involuntary muscle movements (especially of the shoulder and facial
muscles)
iii. Walking aimlessly or in to objects
iv. Occasionally periods of excitement or intense pruritus
• The acute phase is followed by depression with increasing incoordination,
paralysis, coma and death. Case fatality rates are much higher with EEE (up
to 90%) compared to WEE (20–30%).

10. • Clinical signs of VEE encephalitis are similar to those above, although
mortality rate is lower. There is a second clinical syndrome in which
signs are more attributable to generalised infection:
i. Fever
ii. Weakness
iii. Depression
iv. Anorexia
v. Colic
vi. Diarrhoea

11. Post-mortem findings
• There are no characteristic gross lesions. Histologically, changes are
seen in the central nervous system. With VEE, necrotic foci may be
seen in internal organs such as pancreas, liver and heart.

12. Differential diagnosis
• Japanese encephalitis
• Rabies
• Borna disease
• Tetanus
• Botulism
• Lead poisoning
• Hepatic encephalopathy

13. Specimens required for diagnosis
• Blood samples (50 ml) should be collected from febrile horses in the
acute stage of the disease for virus isolation.
• Brain tissue — specimens of cerebral cortex, medulla, pons and
cerebellum — is best collected from horses killed in the acute stage of
the disease, or from horses within 24 hours of death. These should be
put in sterile containers with duplicate specimens collected into neutral
buffered formalin for histopathology.
• Blood samples (20 ml) from horses in the acute and convalescent
stages of the disease for serology, an ELISA test is available.

14. Treatment
• Treatment of viral encephalitis is supportive, because there are no specific
antiviral therapies. Management is focused on controlling pain and
inflammation, preventing injuries associated with ataxia or recumbency, and
providing supportive care. Intervention does not appear to significantly affect
the outcome of most fulminate EEEV infections. For WNV, flunixin
meglumine (1.1 mg/kg, IV, bid) early in the course of the disease decreases the
severity of muscle tremors and fasciculations within a few hours of
administration.
• Recumbent horses that are mentally alert frequently thrash, causing self-
inflicted wounds and posing a risk to personnel. Responses to tranquilizers and
anticonvulsant medications are variable, depending on the virus and severity of
disease. A sling and hoist may be used to assist horses that are recumbent and
have difficulty rising; however, recumbent horses with EEEV generally are too
comatose to sling. Dysphagic horses require fluid and nutritional support.

15. • Until equine protozoal myeloencephalitis is excluded, prophylactic
antiprotozoal medications may be instituted. Other supportive
measures (eg, oral and parental fluids and nutrition for dehydrated and
dysphagic horses) are also important. Broad-spectrum antibiotics
should be given for treatment of wounds, cellulitis, and pneumonia.
Horses with intermittent or focal neuropathies have a better prognosis
than those with complete flaccid paralysis or that appear comatose.
Efficacy of specific antiviral agents for treatment of naturally
occurring WNV or EEEV infection is unknown, even in people.
Recent work with passive immunotherapy indicates possible benefit
after the onset of clinical signs in WNV models.

16. Prognosis
• Mortality of horses showing clinical signs from EEEV is 50%–90%,
from WEEV 20%–50%, from VEEV 50%–75%, and from flavivirus
infections 35%-45%.
• Horses with clinical neurologic signs from alphavirus infection that
recover have a high incidence of residual neurologic deficits, whereas
many horses that recover from WNV disease have been reported to
have no residual neurologic deficits
• In EEEV infection, death is frequently spontaneous. With WNV
disease, horses are euthanized for humane reasons, but spontaneous
death does occur. In EEEV, most surviving horses exhibit longterm
neurologic signs. In WNV disease, overt clinical signs in horses that
recover can last from 1 day to several weeks; improvement usually
occurs within 7 days of onset of clinical signs.

17. Control / vaccines
• Inactivated and attenuated vaccines are available either monovalent or
polyvalent for each of the viruses. In endemic areas, annual
vaccination is recommended.
• Vaccination programs should be supported by mosquito control
programs where practicable.

18. Vaccine for Encephalomyelitis Vaccination on subcutaneous layer

19. Prevention Measures
• Vaccination against alphaviruses and flaviviruses as core annual vaccines are
considered the standard of care for all horses
• Formalin-inactivated whole viral vaccines for EEEV, WEEV, and VEEV are
commercially available in bi- and trivalent forms, usually formulated with
tetanus toxoid
• Mares should be vaccinated 1 mo before foaling to induce colostral antibody
• Protection of horses from arboviruses must also include efforts to minimize
exposure to infected mosquitoes and includes applying an insect repellent that
contains permethrin on the horses at least daily during vector season,
especially at times of day when mosquitoes may be most active
• Environmental management is also essential and includes keeping the barn
area, paddocks, and pastures cleared of weeds and organic material, such as
feces, that might harbor adult mosquitoes. Cleaning water tanks and buckets at
least weekly will reduce mosquito breeding areas

20. Zoonotic Risk
• The reporting of these diseases (or suspicion of such) on an
international and national basis is a basic duty of all veterinarians to
ensure the health and safety of horses and people. As such, a thorough
diagnostic investigation to confirm these infections is imperative,
irrespective of state resources available for subsidized testing.
• People may be infected by most of the arboviruses that commonly
cause viral encephalitis in horses. Clinical signs in people vary from
mild flu-like symptoms to death. Children, the elderly, and those who
are immunosuppressed are the most susceptible
• People with neurologic disease due to arboviruses usually have
permanent neurologic impairment after recovery. Human disease is
reported infrequently and generally follows equine infections by ~2
wk

21. • Veterinarians should be aware of the possibility of human infection
and use repellents and other procedures to protect themselves from
hematophagous insects when working in sylvatic virus habitats or
handling viremic horses. In addition, waterproof clothing (gown,
boots, gloves), respirator (N-95 or N-99 mask), face shield, and hair
covering are recommended during all necropsies performed on horses
suspected of having encephalomyelitis.

22. References
• Equine Enephalomyelitis, In Merck Veterinary Manual, National
Publishing Inc. Eight ed, 1998, Philadelphia, p 931-934
• http://lrd.spc.int/ext/Disease_Manual_Final/b204__equine_viral_ence
phalomyelitis.html
• https://www.msdvetmanual.com/nervous-system/equine-arboviral-
encephalomyelitis/overview-of-equine-arboviral-encephalomyelitis
• https://www.gov.scot/publications/equine-viral-encephalomyelitis/
• Office International des Epizooties, 2002
• https://wwwnc.cdc.gov/eid/article/14/3/07-0816_article