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

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Dunowska M (2016)How common is equine herpesvirus type 1 infection?Vet Rec 178(3), 67-69 PubMed.
  • Barbic Let al(2012) Two outbreaks of neuropathogenic equine herpesvirus type 1 with breed-dependent clinical signs.Vet Rec170(9), 227 PubMed.
  • Goehring L E, Landolt G A & Morley P S (2010)Detection and management of an outbreak of equine herpesvirus type 1 infection and associated neurological disease in a veterinary teaching hospital.J Vet Intern Med24(5), 1176-1183 PubMed.
  • Goehring L Eet al(2010)Experimetnal infection with neruopathogenic equine herpesvirus type 1 (EHV-1) in adult horses.Vet J186(2), 180-187 PubMed.
  • Kydd J H, Slater J, Osterrieder N, Antezak D F & Lunn D P (2010)Report of the second Havermeyer EHV-1 workshop, Steamboat Springs, Colorado, USA, September 2008.Equine Vet J42(6), 572-575 PubMed.
  • Pronost Set al(2010)Relationship between equine herpesvirus-1 myeloencephalopathy and viral genotype.Equine Vet J42(8), 672-674 PubMed.
  • Nugent J & Paillot R (2009)Equine herpes myeloencephalopathy: unravelling the enigma.Vet J180(3), 271-272 PubMed.
  • Pusterla N, Wilson W B, Madigan J E & Ferraro G L (2009)Equine herpesvirus-1 myeloencephalopathy: a review of recent developments.Vet J180, 279-289 PubMed.
  • Allen G Pet al (2008)Prevalence of latent, neuropathogenic equine herpesvirus-1 in the Thoroughbred broodmare population of central Kentucky.Equine Vet J40(2), 105-110 PubMed.
  • Gilkerson J R (2008)Equine herpesvirus neurological disease.Equine Vet J40(2), 102-103 PubMed.
  • Leutenegger C M, Madigan J E, Mapes S, Thao M, Estrada M & Pusterla N (2008)Detection of EHV-1 neuropathogenic strains using real-time PCR in the neural tissue of horses with myeloencephalopathy.Vet Rec162(21), 688-690 PubMed.
  • Paillot R, Case R, Ross J, Newton R & Nugent J (2008)Equine herpes virus-1: virus, immunity and vaccines.Open Sci J2, 68-91 VetMedResource.
  • Henninger R Wet al(2007)Outbreak of neurologic disease caused by Equine herpesvirus-1 at a University Equestrian Center.J Vet Intern Med21, 157-165 PubMed.
  • Luce Ret al(2007)Equine herpesvirus-1-specific interferon gamma (IFNy) synthesis by peripheral blood mononuclear cells in Thoroughbred horses.Equine Vet J39(3), 202-209 PubMed.
  • Allen G P (2006) Antemortem detection of latent infection with neuropathogenic strains of equine herpesvirus-1 in horses.Am J Vet Res67(11), 1820 PubMed.
  • Borchers K, Thein P & Sterner-Kock A (2006)Pathogenesis of equine herpesvirus-associated neurological disease and dysfunction: a revised explanation.Equine Vet J38(3), 283-287 PubMed.
  • Hahn C (2006)The wobbly horse: differential diagnoses.In Pract28(1), 8-13 VetMedResource.
  • Hussey S Bet al(2006)Detection and quantification of equine herpesvirus-1 viremia and nasal shedding by real-time polymerase chain reaction.J Vet Daign Invest18(4), 335-342 PubMed.
  • Goehring L Set al(2001)The mystery of equine herpes myeloencephalopathy.Equine Vet Educ13(1), 36-42 VetMedResource.
  • Donaldson M T and Sweeney C R (1998)Herpesvirus myeloencephalopathy in horses, 11 cases.JAVMA213(5), 671-675 PubMed.
  • Wilson W D (1997)Equine herpesvirus infections and EHV-1 myeloencephalopathy.Vet Clin North Am Equine Practice13(1), 53-72 PubMed.
  • Ostlund E N (1993)The Equine herpesviruses.Vet Clin North Am Equine Pract9(2), 283-294 VetMedResource.

Other sources of information

  • Horserace Betting Levy Board (2016)Codes of Practice.5th Floor, 21 Bloomsbury Street, London WC1B 3HF, UK. Tel: +44 (0)207 333 0043; Fax: +44 (0)207 333 0041; Email:enquiries@hblb.org.uk; Website:http://codes.hblb.org.uk.Wilkins P A, Henninger R, Reed S M & Del Piero F (2003)Acyclovir as Treatment for EHV-1 Myeloencephalopathy.In:Proc 49th AAEP Convention.pp 394-396.
  • Reed S M, Saville W J A & Schneider R K (2003)Neurologic Disease: Current Topics In-depth.In:Proc 49th AAEP Convention.pp 243-258.


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