Saturday 11 May 2013

Equine Neurological Disease



Diagnosis is based on a few techniques:


  • History- geographical location and recent travel. Determine onset and duration of clinical signs. Information of health status of other horses in the vicinity. Vaccination history. 
  • Clinical exam- normally fever coinciding with viraemia, virus replication at entry site or specific organ infection. Symmetrical, multifocal or diffuse lesions. 
  • CSF analysis and serology- key in viral encephalitis. Mononuclear pleocytosis and increased protein concentration commonly. Identify ag/ab via culture, PCR and ab detection tests e.g. ELISA. 
  • Medical imaging and functional testing- CT, MRI or EEG. Limited. Only head and up to mid cervical region and usually non specific intracranial oedema. 
  • Post mortem exam- histopathology, immunohistochem or PCR amplification. 
General treatment Reccomendations:
  • Fever and neurological signs- infectious unless proven otherwise so isolate. 
  • Quiet, dark stable with deep bedding and padded walls. 
  • Recumbent= turn every 4-6 hours.
  • NSAIDS, antivirals (valacyclovir), ag specific therapy e.g. WNV and vitamin E/thiamine. 
  • Prevention- vaccination/minimise exposure to vector/reservoir. 
Equine Herpes Virus 

EHV-1
  • Alpha herpes virus.
  • Enveloped DNA virus.
  • Latent infection.
  • Humoral immunity short lived.
  • Naturally low ab levels. 
Can occur sporadically or as outbreaks. 

  • 85% morbidity, 10% mortality. Myeloencelopathy. Also associated with respiratory disease and abortion. 
  • Clinical signs result of vasculitis and thrombosis of arterioles in the brain and spinal cord. May be a recent history of abortion/respiratory disease on the premises. 
  • Sudden onset and early sign stabilization- Ataxia (hindlimbs or all) to recumbency, cauda equina signs atony of bladder, flaccid tail and anus and perineal hypoalgesia. Occasional cranial nerve involvement. 
Diagnosis:
  • Virus isolation/PCR-> nasal swab, buffy coat or CSF.
  • Serology-> complement fixation/ELISA. 4 fold titre rise.
  • CSF-> xanthochromia. 
EHV-1- possible neurovirulent form. New infection from respiratory outbreak or reactivation of latent virus under times of stress (less likely with neurological form). 

Management:
  • Isolate.
  • Prognosis reasonable with good nursing- recovery day to weeks. Poor prognosis if recumbent more than 24 hours. 
  • Recurrence of neurological signs unreported.
  • Vasculitis-> antinflammatories, NSAIDS, corticosteroid and aspirin. 
Prevention:
  • Vaccination against EHV1 and 4. Ineffective against neurological form.
  • Could possibly worsen neurological disease (if immune mediated). 
Rabies
  • ssRNA with envelope.
  • Transmitted by saliva/contaminated bite wounds. 
  • Uncommon.
  • Zoonosis.
  • Salivary/droplet transmission- carnivore bites to limbs.
Pathogenesis:
  • Local inoculation at wound.
  • Peripheral nerve access.
  • Gradual/slow movement centrally (centripetal axoplasmic flow). 
  • Replication in spinal/dorsal root ganglia.
  • Rapid CNS spread- spinal cord. 
  • Centrifugal spread down nerves to salivary glands.
Incubation period variable. Dependent on virus, strain, and size of inoculum and proximity to CNS.

No pathognomic signs.

  • Spinal form-> paralytic.
  • Brain stem-> dumb.
  • Cerebrum-> furious. 
Spinal/paralytic form:
  • Most common.
  • Localised hyperaesthesia,- self mutilation and close to inoculum site.
  • Progressive ascending- weakness, ataxia and lameness.
  • 3-5 day recumbency. 
Dumb/brainstem form or furious/cerebrum form:
  • Unusual in horses.
Diagnosis:
  • Difficult- vague signs.
  • Assumption of rabies in endemic areas.
  • Rapid progressive neurological signs.
  • PM-> negri bodies within neurones. Flourescent ab. Zoonotic- beware. 
Treat:
  • 100% fatal.
  • Kill on suspicion- early diagnosis essential.
  • Limit human contact. 
Control/Prevention:
  • Vaccination very effective (annual in epidemic areas). 
  • Horses rarely infect other animals.

Arbovirus- West Nile Virus
  • Flavivirus.
  • Replicates in birds- reservoir.
  • Mosquitoes transfer virus from reservoir to number of species. 
  • Horse/human terminal host. 
Pathogenesis:
  1. Initial virus replication at inoculum site.
  2. Viraemia-> signs of uncomplicated inf-> fever, depression and anorexia. 
  3. Some horses-> virus enters the CNS, this results in diffuse or multifocal encephalomyelitis and involvement of the spinal cord is common. 
Neurological Signs
  • Muscle fasciculations over entire body.
  • Weakness, ataxia and dysmetria.
  • Cranial nerves affected sometimes.
  • Mentation affected (intracranial oedema).
  • Sudden death in some horses.
Treatment:
  • Hyperimmune plasma specific to WNV available in USA. 
  • Supportive care. NSAIDS, mannitol (decreases oedema) and perhaps corticosteroids. 
Diagnosis:
  • ELISA ag specific testing.
  • PM-> virus culture of brain material, and immunohistochemistry. 
Prognosis-> few cases gradually resolve-> long term neurological deficits. 

Prevention:
  • Reduce vector contact via environment and repellents. 
  • USA- vaccine. 





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