- Non-supprative viral encephalitis of horses, birds and humans that is transmitted by mosquitoes ( Culex tarsalis and Culiseta melanura ) [Equine viral encephalitides] .
- The virus is maintained in sylvatic populations of wild birds.
- Cause : virus from:
- Family: Togaviridae .
- Genus: Alphaviridae .
- Group A Arboviruses (closely related EEE [Eastern Equine Encephalomyelitis virus] and VEE viruses). Transmitted from sylvatic populations of wild brids to hroses via blood meal from mosquito bite. Virus over winters in other mammals, birds, amphibians and reptiles (reservoir hosts).
- Signs : biphasic fever (38-41°C, 2 and 6 days), then general depression, dullness, anorexia, stiffness, ataxia, hyperesthesia, aggression, excitability, continuous chewing movements, aimless wandering, somnolence → head pressing, circling, twitching, recumbency and death.
- Diagnosis : paired serum titers (4-fold increase in titer over 2-4 weeks), virus isolation from brain tissue at necropsy or single high serum titer during the acute phase of the disease.
- Treatment : no specific antiviral treatment is available to treat WEE. Therefore, supportive care, nursing care, prevention of self-trauma, and non-steroidal anti-inflammatory therapy, fluids, electrolytes, total and partial parental nutrition, DMSO and corticosteroids (controversial). Also, diazepam or phenobarbital to control convulsions.
- Prognosis : guarded as mortality rates range from 10-50% in cases with neurologic signs. Once recumbent, death may occur within 5 days. Horses that recover from clinical disease frequently have persistent neurologic deficits.
- Rabies (in rabies endemic areas) .
- EEE (endemic areas) [Eastern Equine Encephalomyelitis] .
- VEE (endemic areas).
- Equine herpesvirus myeloencephalopathy [CNS: myeloencephalopathy - EHV] .
- West nile virus encephalitis .
- The infection may be cleared by the immune response and no disease seen (this may happen 50-90% of all WEE infections) or the disease may progress to clinical encephalitis with signs of aggressiveness, irritable behavior, somnolence and non-responsiveness.
- Horses may exhibit hyperesthesia, self-mutilation, head pressing, aimless wandering, compulsive walking, blindness and a negative menace response.
- Facial paralysis.
- Pharyngeal paralysis.
- Severe ataxia and paresis in all four limbs, progressing to recumbency, coma and death.
- More horses recover from WEE infection compared to EEE and VEE infections (20-50% mortality).
- Guarded to poor: mortality is 20-50% in horses infected with WEE.
- Recovered horses often have residual neurologic deficits such as ataxia, weakness, somnolence and abnormal behavior.
- Complete recovery is more likely in WEE than EEE infections.
- Serum antibodies from natural infection last for up to 2 years after recovery.
Expected response to treatment
- Treatment is more often effective in decreasing mortality in WEE compared to EEE infections.
- Once the horse becomes recumbent, death usually ensues within 5 days.
Reasons for treatment failure
- There are no specific antiviral treatments for WEE and supportive treatment is often not effective in reversing the severe neurologic deficits.
- Once the horse becomes recumbent, management is difficut due to its size.