Western Equine Encephalomyelitis

Introduction

• 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. 

Diagnosis

Differential diagnosis

• Rabies (in rabies endemic areas)    .
• Trauma.
• EEE (endemic areas)  [Eastern Equine Encephalomyelitis]  .
• VEE (endemic areas).
• Equine herpesvirus myeloencephalopathy     [CNS: myeloencephalopathy - EHV]  .
• West nile virus encephalitis    .

• Hepatoencephalopathy.

• Equine protozoal myeloencephalitis    .
• Brain abscess.
• Leukoencephalomalcia.
• Verminous encephalitis    .

• Neoplasia.

Diagnosis

Clinical signs

• Fever.
• Lethargy.
• Stiffness.
• Lymphadenopathy.

• Anorexia.
• Depression.
• Tachycardia. 
• 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.

• Nystagmus.
• Facial paralysis.
• Pharyngeal paralysis.
• Dysphagia.
• 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).

• Seizures.
• Convulsions.

Outcomes

Prognosis

• 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.