no edit summary
Line 2: Line 2:     
====Description====
 
====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
+
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====
 
====Epidemiology====
Line 9: Line 9:     
====Signalment====
 
====Signalment====
  −
====Diagnosis====
  −
Clinical signs.  Virus isolation can be performed from blood or spinal fluid
      
====Clinical Signs====
 
====Clinical Signs====
Line 53: Line 50:  
*Drooping eyelids
 
*Drooping eyelids
 
*Incoordination
 
*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====
 
====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.
 
====Biopsy====
 
====Biopsy====
   −
====Pathology====
+
====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 ofthe 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 myoencephalopathy (EPM)
 +
*Verminous encephalitis
 +
*West Nile Virus (WNV) infection
 +
*Toxicosis
 +
 
    
====Treatment====
 
====Treatment====
    
====Prognosis====
 
====Prognosis====
Often '''fatal''', comatose animals rarely survive.  Survivors exhibit functional improvement over weeks to months.
+
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====
 
====Control====
 
Annual '''vaccination'''.  Vector control.  Human vaccination recommended for vets in endemic areas
 
Annual '''vaccination'''.  Vector control.  Human vaccination recommended for vets in endemic areas
1,406

edits