Equine Togaviral 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. Central nervous system (CNS) replication within a week
Aetiology
Epidemiology
Disease associated with EEE, WEE and VEE is largely restricted to the Western Hemisphere, ranging from temperate to desert climates. EEE in the United States is mainly seen in the Southeastern United States but has been detected in all states east of the Mississippi River and some Western states. Large outbreaks of WEE have been described in California and other Western states but the incidence of clinical disease in these areas has experienced a dramatic decrease. The reason for this unknown but may be due to geographical variation in virulence. Equine disease associated with WEE is rare on the Eastern seaboard ofthe United States. VEE virus is a very important human andveterinary pathogen in the Western Hemipshoere that can cause large outbreaks of disease in humans and horses over large geopgrahic areas. Transfer is via vector: mostly through mosquito salivary transfer. WEE and VEE may also be transmitted via nasal secretions but this is less likely. Disease amplification occurs during the viraemic phase which lasts until nervous signs develop. Amplification from horses is unlikely with EEE and WEE but occurs with VEE in association with a relatively high viraemia. Ocular and nasal discharges from infected horses cotnain high concentrations of VEE. Zoonotic spread has been noted with VEE but is unlikely for the other two serotypes. Horse to horse spread of EEE is possible. Humans and horses are terminal hosts for WEE. Horses with WEE are sentinels for humans in a given area.
Seasonal Incidence
The diseases occur largely during the height of the vector season. In temperate climates, case numbers peak in June to November. In warm climates, where the vector season is longer, the disease period is prolonged. Global warming may promote more cold climate outbreaks.
Pathogenesis
After inoculation into an equine host, viruses multiply in the muscle, enter the lymphatic circulation and localize in lymph nodes. Viral replication occurs in macrophages and neutrophils with subsequent shedding and significant clearance of viral particles. No further clinical signs develop if clearance is successful but neutralizing Abs are still produced. Viral immunological avoidance mechanisms include erythrocyte and leukocyte absorption. After incomplete elimination, residual virus infects endothelial cells and concentrates in highly vascular organs such as the liver and spleen. In these organs, viral replication produces circulating virus. The second viraemic period is typically associated with early clinical signs. CNS infection occurs within 3-5 days.
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
| Also known as: | Equine viral encephalitis, Equine viral encephalomyelitis Equine viral encephalitides, Equine viral encephalomyelitides |