Equine Togaviral Encephalitis

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. Central nervous system (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.

Pathogenesis

See this page for details on pathogenesis.

Signalment

Unvaccinated adult horses are at risk in areas with suitable vectors. Vaccinated horses can still develop the disease, particularly if they are young or old.

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

Diagnosis

Presumptive based on clinical signs and epidemiological features. Definitive diagnosis requires serological tests and/or post-mortem examination. Virus isolation can be performed from blood or spinal fluid samples

Laboratory Tests

A combination of complement fixation (CF), haemagglutination inhibition (HAI) and cross-serum neutralization assays supports the acquisition of a positive diagnosis. A 4-fold increase in antibody (Ab) titre in convlescent sera is quoted for diagnosis but this test lacks sensitivity. The presence of viral Abs within 24hours of the initial viraemia typically precedes clinical signs. Ab titre increases sharply then deteriorates over 6 months. Samples taken when clinical signs appear are likely to miss the Ab peak and may thus demonstrate a decreasing titre. A single sample demonstrating an increased titre using HAI, CF and neutralizing Ab can provide a presumptive diagnosis.

Viral-specific IgM to the surface glycoprotein of Venezuelan EEV may be detected by ELISA, from 3 days post-onset of clinical signs up to 21 days post-infection. The ELISA is useful in acute VEE infections where convalescent serum samples are unobtainable. Viral culture may also be useful for acute VEE. Virus may be isolated from the CSF of acutely infected horses. Virus may be found in brain tissue using fluorescent Ab, ELISA and virus isolation.

Maternal-derived Ab may interfere with diagnosis in foals. The serum half-life of colostral Ab in foals is around 20days.

Clinical Pathology

Changes in cerebrospinal fluid (CSF) include increased cellularity (50-400 mononuclear cells per microlitre) and protein concentration (100-200mg/dl)

Post-mortem findings

PRECAUTION: infective viral particles may be present in CNS and other tissues. The brain and spinal cord are typically grossly normal, but vascular congestion and discolouration of the CNS may be seen. Histologically the entire brain is affected by nonseptic mononuclear cell and neutrophilic inflammation. Severe lesions are noted in the cerebral cortex, thalamus and hypothalamus. Mononuclear meningitis, neuronal degeneration, gliosis and perivascular cuffing with mononuclear cell and neutrophilic infiltration are evident. Immunohistochemistry can be diagnostic. Liquefactive necrosis and haemorrhage of the cerebral cortex, atrophy of the pancreatic acinar cells and hyperplasia of the pancreatic duct cells commonly occur with VEE.

Differential diagnosis

• Other togaviral encephalitides
• Trauma
• Hepatic encephalopathy
• Rabies
• Leukoencephalomalacia
• Bacterial meningoencephalitis
• Equine protozoal myeloencephalitis (EPM)
• Verminous encephalomyelitis
• West Nile Virus (WNV) infection
• Toxicosis

Treatment

No effective, specific treatment is available. Supportive management includes:

• NSAIDs (phenylbutazone, flunixin meglumine) to control pyrexia, inflammation and discomfort
• DMSO IV in a 20% solution to control inflamation, provide some analgesia and mild sedation
• Pentobarbital, diazepam IV, phenobarbital PO or phenytoin IV to control convulsions
• Antibiotic therapy in cases with secondary bacterial infection
• Balanced fluid solutions IV or PO as necessary to correct hydration status
• Dietary supplementation (enteral or parenteral if anorexia persists more than 48 hours)
• Laxatives to minimize the risk of impaction
• Protection of areas susceptible to self-induced trauma and provision of deep bedding
• Sling support if the horse is recumbent

Prognosis

Comatose animals rarely survive. Survivors exhibit functional improvement over weeks to months, but complete recovery from neurological deficits is rare. Residual ataxia, depression and abnormal behaviour is often seen with EEE, less commonly with WEE. The mortality rates for neurological equine viral encephalitis are reportedly:

• EEE 75-100%
• WEE 20-50%
• VEE 40-80%

It is generally assumed that infection does not provide protective immunity, however, protection for up to 2 years has been noted.

Control

Vaccination

Vaccinate susceptible horses annually. Vaccinate horses in the face of an outbreak. Vaccinate mares one month prior to foaling. Colostral-derived Ab persists for 6-7 months. Although folas ca be vaccinated at any time, they should be re-vaccinated at 6 months and at one year if they were vaccinated early. Most vaccines are killed (inactivated formalin) and elicit significant increases in Ab titre after 3 days. Protective titres last for 6-8 months. Some cross-protection is seen between the serotypes but not between WEE and EEE. Monovalent, divalent and trivalent vaccines are available but the response to VEE vaccination alone is decreased in horses previously vaccinated against WEE and EEE. Susceptible horses should be vaccinated annually in late spring or several months before the high risk season. Biannual or triannual vaccination is recommended in regions where the mosquito season is prolonged. Vaccination does not interfere with the ELISA assay for VEE. PRECAUTION: human vaccination recommended for vets in endemic areas.

Vector control

Responsible use of insecticides and repellents, elimination of standing water and stable screening will all help to reduce viral transmission. Environmental application of insecticides may be useful in endemic areas or during an outbreak. Horses infected with Venezuelan EEV should be isolated for 3 weeks after complete recovery and such cases are reportable in the United States.

References

VEE in Donkeys

Also known as:

Equine viral encephalitis, Equine viral encephalomyelitis Equine viral encephalitides, Equine viral encephalomyelitides Eastern equine encephalitis, Eastern equine encephalomyelitis, EEE Western equine encephalitis, Western equine encephalomyelitis, WEE Venezuelan equine encephalitis, Venezuelan equine encephalomyelitis, VEE