Equis ISSN 2398-2977

CNS: myeloencephalopathy - EHV

Synonym(s): EHV-1, myeloencephalopathy, herpes myelitis

Contributor(s): Frank Andrews, Rachael Conwell, Cody Coyne, Robert J MacKay, Michael Porter, Vetstream Ltd

Introduction

  • Occasional outbreaks or sporadic cases of neurologic syndromes associated with equine herpesvirus (EHV) infection.
  • Cause: EHV-1   Equine herpesvirus  .
  • Signs: fever, depression, acute/subacute onset of ataxia and paresis, urinary incontinence   Incontinence  , abortion   Abortion: EHV-1  , neonatal sepsis and respiratory disease   Respiratory: EHV infection  .
  • Diagnosis: RT-PCR (whole blood or nasal secretions), CSF analysis, virus isolation and paired serology (virus neutralizing antibody detection).
  • Treatment: supportive; good nursing essential; corticosteroids may be beneficial in early stages; +/- antiviral agents.
  • Prognosis: dependent on severity of clinical signs - most horses recover within days to months with good nursing; severely affected/recumbent animals may die (10% mortality rate reported in clincially affected horses) or require euthanasia   Euthanasia  .
  • See also:
Print off the Owner factsheet on Equine herpesvirus - EHV to give to your clients.

Pathogenesis

Etiology

Pathophysiology

  • Immune-mediated ischemic vasculitis of small blood vessels in brain, brainstem and spinal cord   →   neurological signs.
  • Reactivation of latent EHV-1 infection   →   neurologic signs.
  • Neurotropic strain of EHV-1 may act directly on CNS. The "Neurotropic strain" has a single point mutation in the DNA sequence which may impart increased virulence compared to the EHV-1 strain described in the past. It has been identified as sequence variation in the DNA polymerase gene (ORF 30) involved in initial viral replication. This increased virulence has resulted in significant increase in morbidity and mortality during recent outbreaks.
  • Type III and cell-mediated hypersensitivity reactions occur   →   immune-mediated vasculitis rather than direct infection of neural tissues   →   localized ischemia of spinal cord, brain.
  • Ischemic necrosis of gray and especially of white matter occurs.
  • Immune response often fails to eliminate virus; following clinical disease, most horses have a latent infection.
  • Recent investigations suggest that complement activation and, microvascular thrombus formation are probably the most important factors contributing to the molecular pathogenesis of the disease and the creation of ischemic spinal cord lesions. 
  • Virus has a tropism for vascular endothelium and vascular myocytes and is delivered intracellularly to affected sites by virus-ladened leukocytes.
  • Induced expression of cellular adhesion molecules on the membrane surface of both leukocytes and vascular endothelium facilitates the transfection of viral agents from leukocytes to the vascular endothelium.
  • Endothelial cell death ensues followed by intravascular thrombosis, secondary to the release of pro-coagulant components (tissue thromboplastin).
  • In the neurologic form of EHV disorders, there is no evidence of direct neuronal invasion by the viral agent in contrast to neurologic herpes conditions affecting other species.

Timecourse

  • Incubation 2-8 days.
  • Following initial exposure, EHV-1 may develop into a latent infection and remain in a dormant state for an extended period of time. Reactivation occurs due to stress, administration of corticosteroids.
  • Once fever develops, clinical signs may worsen quickly within 1-7 days   →    severe neurologic signs and potentially death.
  • With appropriate treatment and nursing, clinical improvement can be seen within several days of development of neurological signs, but recumbent horses with severe neurological disease are unlikely to survive.
  • Complete recovery from neurologic signs is possible but may take up to a year and, in some horses, abnormalities will remain.

Epidemiology

  • EHV-1 is a ubiquitous equine viral pathogen.
  • Myeloencephalopathy is a sporadic and relatively uncommon manifestation.
  • Outbreaks can occur at riding schools, racing training yards, equine veterinary hospitals.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

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