Difference between revisions of "Equine Viral Encephalitis"
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| − | == | + | ====Description==== |
| − | + | Viraemia during the acute phase of EEE and WEE. Incubation period of 1-3weeks after experimental infection with EEE or WEE. Incubtion often shorter with EEE. CNS replication within a week | |
| − | == | + | ====Epidemiology==== |
| − | + | Transfer via '''vector''': mostly through '''[[Culicidae|mosquito salivary transfer]]''' | |
| + | Disease amplification occurs during the viraemic phase which lasts until nervous signs develop. | ||
| − | + | ====Signalment==== | |
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| − | + | ====Diagnosis==== | |
| − | + | Clinical signs. Virus isolation can be performed from blood or spinal fluid | |
| − | == | + | ====Clinical Signs==== |
| − | + | Worse in unvaccinated animals. Acute signs of EEE and WEE are nonspecific, last up to 5 days and include: | |
| + | *mild to severe pyrexia | ||
| + | *anorexia | ||
| + | *stiffness | ||
| + | Early signs transient and often missed: | ||
| + | *pyrexia | ||
| + | *mild depression | ||
| + | Disease progression occurs more frequently with EEE than WEE: | ||
| + | *fever may rise and fall sporadically | ||
| + | Cerebral signs often occur a few days post-infection (but can occur at any time. In the acute phase the following may be noted: | ||
| + | *propulsive walking | ||
| + | *depression | ||
| + | *somnolence | ||
| + | *hyperaesthesia | ||
| + | *agression | ||
| + | *excitability | ||
| + | *frenzy in response to sensory stimulation | ||
| + | *conscious proprioceptive deficits | ||
| + | With progression, worsening cerebral cortical and cranial nerve dysfunction may result in: | ||
| + | *head pressing | ||
| + | *propulsive walking | ||
| + | *blindness | ||
| + | *circling | ||
| + | *head tilt | ||
| + | *facial and appendicular muscle fasciculations | ||
| + | *paralysis of pharynx, larynx and tongue | ||
| + | *recumbency for 1-7 days followed by death | ||
| + | VEE may have similar or different clinical presentations to WEE and EEE, which may relate to a persistently hightitre viraemia with VEE and differences in strain pathogenicity: | ||
| + | *pyrexia peaks early and remains high throuhgout the disease course | ||
| + | *mild fever and leukopenia associated experimentally with endemic strains | ||
| + | *severe pyrexia and leukopenia associated with epidemic strains | ||
| + | *diarrhoea, severe depression recumbency and death may precede neurological signs | ||
| + | *neurological signs around 4 days post-infection | ||
| + | *other associated signs: abortion, oral ulceration, pulmonary haemorrhage, epistaxis | ||
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| − | + | *Paralysis of the lips | |
| − | + | *Drooping eyelids | |
| + | *Incoordination | ||
| + | ====Laboratory Tests==== | ||
| − | + | ====Biopsy==== | |
| − | + | ====Pathology==== | |
| − | [[Category: | + | ====Treatment==== |
| − | [[Category: | + | |
| + | ====Prognosis==== | ||
| + | Often '''fatal''', comatose animals rarely survive. Survivors exhibit functional improvement over weeks to months. | ||
| + | |||
| + | ====Control==== | ||
| + | Annual '''vaccination'''. Vector control. Human vaccination recommended for vets in endemic areas | ||
| + | |||
| + | ====References==== | ||
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| + | |||
| + | '''[[Venezuelan Equine Encephalomyelitis (VEE) - Donkey|VEE in Donkeys]]''' | ||
| + | |||
| + | [[Category:Togaviridae]] | ||
| + | [[Category:Horse]] | ||
| + | [[Category:To_Do_-_Viruses]] | ||
| + | [[Category:To_Do_-_Nina]] | ||
Revision as of 14:50, 6 July 2010
 |
This article is still under construction. |
Description
Viraemia during the acute phase of EEE and WEE. Incubation period of 1-3weeks after experimental infection with EEE or WEE. Incubtion often shorter with EEE. CNS replication within a week
Epidemiology
Transfer via vector: mostly through mosquito salivary transfer Disease amplification occurs during the viraemic phase which lasts until nervous signs develop.
Signalment
Diagnosis
Clinical signs. Virus isolation can be performed from blood or spinal fluid
Clinical Signs
Worse in unvaccinated animals. Acute signs of EEE and WEE are nonspecific, last up to 5 days and include:
- mild to severe pyrexia
- anorexia
- stiffness
Early signs transient and often missed:
- pyrexia
- mild depression
Disease progression occurs more frequently with EEE than WEE:
- fever may rise and fall sporadically
Cerebral signs often occur a few days post-infection (but can occur at any time. In the acute phase the following may be noted:
- propulsive walking
- depression
- somnolence
- hyperaesthesia
- agression
- excitability
- frenzy in response to sensory stimulation
- conscious proprioceptive deficits
With progression, worsening cerebral cortical and cranial nerve dysfunction may result in:
- head pressing
- propulsive walking
- blindness
- circling
- head tilt
- facial and appendicular muscle fasciculations
- paralysis of pharynx, larynx and tongue
- recumbency for 1-7 days followed by death
VEE may have similar or different clinical presentations to WEE and EEE, which may relate to a persistently hightitre viraemia with VEE and differences in strain pathogenicity:
- pyrexia peaks early and remains high throuhgout the disease course
- mild fever and leukopenia associated experimentally with endemic strains
- severe pyrexia and leukopenia associated with epidemic strains
- diarrhoea, severe depression recumbency and death may precede neurological signs
- neurological signs around 4 days post-infection
- other associated signs: abortion, oral ulceration, pulmonary haemorrhage, epistaxis
- Paralysis of the lips
- Drooping eyelids
- Incoordination
Laboratory Tests
Biopsy
Pathology
Treatment
Prognosis
Often fatal, comatose animals rarely survive. Survivors exhibit functional improvement over weeks to months.
Control
Annual vaccination. Vector control. Human vaccination recommended for vets in endemic areas