Equis ISSN 2398-2977

CNS: Equine protozoal myeloencephalitis (EPM)

Synonym(s): EPM

Contributor(s): Frank Andrews, Cody Coyne, Robert J MacKay, Graham Munroe, Michael Porter

Introduction

  • Neurologic disorder of horses only found in horses from the Americas.
  • Cause: protozoaSarcocystis neuronaor, less commonly,Neospora hughesi, causing direct neuronal damage or damage secondary to inflammation.
  • Signs: assymetrical weakness, ataxia, vestibular disease (peripheral or central) peripheral neuropathy, ill-defined hindlimb lameness, asymmetric muscle atrophy, signs of brain disease - can mimic almost any neurologic condition.
  • Diagnosis: western blot forS. neuronaorN. hughesiIgG in CSF - post-mortem histopathology, enzyme-linked immunosorbent assays (ELISA).
  • Treatment: anti-protozoal agents, anti-inflammatory drugs.
  • Prognosis: 50-75% improve with treatment, approximately 25% recover completely - dependent upon severity and duration of neurologic signs and speed of diagnosis/treatment.
Print off the Owner factsheet on Equine protozoal myeloencephalitis to give to your clients.

Pathogenesis

Etiology

  • Sarcocystis neurona(protozoan).
  • Neospora hughesi(protozoan).
  • Has an obligate 2-host-species life-cycle.
  • The definitive host is any of 3 opossum species found in the Americas:
    • Didelphis virginiana(USA).
    • D. albiventris.
    • D. marsupialis(central and South America).
  • S. neuronaapparently can use multiple intermediate hosts including the 9-banded armadillo (Novemcinctus dasypus), striped skunk (Mephitis mephitis) and possibly the domestic cat (Felis domesticus) and brown-headed cowbird (Molothrus ater).
  • Horses are an aberrant intermediate host ofSarcocystis neurona.
  • Horses are thought to be dead-end hosts forS. neurona.
  • The hosts forN. hughesiare not known.
  • Ingested sporocysts   →   excyst   →   sporozoites enter horse tissues.
  • Tissue cysts are not formed but in some horses the schizonts and merozoites migrate to the CNS where they continue to undergo asexual reproduction intracellularly in neurons and other cells without forming tissue cysts or being transmitted to other animals.

Predisposing factors

General
  • Exposure to organism is widespread throughout the American continents and matches natural range of opossum closely.
  • Some premises or regions appear to be infected endemically with up to 100% seroprevalence and above-average prevalence of disease.
  • 'Stress' of breaking, training, transportation and previous illness or parturition may be a risk factor for EPM.
  • Chronic exposure to immune suppressive doses of corticosteroids.
  • Serial antibody testing of foals suggest that infection with the organism can occur before the animal reaches 1 year of age.
  • Presence of woodlands and other conditions favorable for opossum habitat are risk factors.

Pathophysiology

  • Ingestion ofSarcocystis neurona  Sarcocystis neurona  sporocysts in some horses   →   merozoites migrating to central nervous system (CNS) where they multiply   →   direct neuronal damage or inflammation   →   variety of clinical signs.
  • Merozoite/schizont migration to peripheral nervous system (PNS) resulting in direct damage to peripheral nerves and subsequent asymmetrical clinical disease.
  • Merozoite/schizont migration to CNS and proliferation within cells   →   cell damage, cell death and a local inflammatory/edematous response.
  • Protozoal proliferation and neurologic dysfunction can occur at any site in the CNS   →   clinical neurologic signs directly referable to these variable/multiple sites.
  • Most seropositive horses probably ingest sporocysts, mount an immune response and clear the organism before it causes clinical signs.
  • Some horses become infected, are unable to mount a suitable immune response (reasons unknown), and develop clinical signs.
  • Lymphocytes from EPM-negative horses respond significantly higher toS. neuronasurface antigen (SnSAG1) than lymphocytes from EPM-positive horses.
  • IFN-g production is detectable by 24 h in lymphocyte cultures in response to cloned antigen (SnSAG1) exposure in the very high percentage of EPM-negative horses.
  • It appears that theS. neuronaparasite is able to induce an immunosuppressive effects towards parasite-derived antigens based on observed declines in parasite-specific immune responses.

Timecourse

  • Ingestion of sporocyst   →   development of clinical signs = >4 weeks (based on experimental trials with high doses of sporocyst).
  • Natural infection, may take up to several years from ingestion of sporocysts to development of clinical signs.
  • Seroconversion againstS. neuronamay take only 3 weeks.

Epidemiology

  • Protozoan parasite encysted in muscle of intermediate host, eg armadillo, skunk   →   eaten by opossums   →   sexual reproduction of organism in intestinal epithelium   →   infective sporocysts in feces   →   fecal contamination of intermediate host's food and water   →   ingestion by intermediate host   →   sarcocysts encysted in muscle.
  • It is likely that horses ingest feed and water contaminated by infected opossum feces and act as an aberrant intermediate host.

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.
  • Dirikolu Let al(2006)New therapeutic approaches for equine protozoal myeloencephalitis: pharmacokinetics of diclazuril sodium salts in horses.Vet Ther7(1), 52-63 PubMed.
  • Furr Met al(2006)Prophylactic administration of ponazuril reduces clinical signs and delays seroconversion in horses challenged withSarcocystis neurona.J Parasitol92(3), 637-643 PubMed.
  • Hahn C (2006)The wobbly horse: differential diagnoses.In Pract28(1), 8-13 VetMedResource.
  • Cutler T Jet al(2001)Immunoconversion againstSarcocystis neuronain normal and dexamethasone-treated horses challenged withS. Neuronasporocysts.Vet Parasitol95(2-4), 197-210 PubMed.
  • Dubey J P, Lindsay D S, Saville W J, Reed S M & Speer C A (2001)A review ofSarcocystis neuronaand equine protozoal myeloencephalitis (EPM).Vet Parasitol95, 89-131 PubMed.
  • MacKay R J, Granstrom D E, Saville W J & Reed S M (2000)Equine protozoal myeloencephalitis.Vet Clin North Am16, 405-425 VetMedResource.
  • Saville W J, Reed S Met al(2000)Analysis of risk factors for the development of equine protozoal myeloenchelphalitis in horses.JAVMA217(8), 1174-1180 PubMed.
  • MacKay R J (1997)Equine protozoal myelencephalitis.Vet Clin North Am Equine Pract13(1), 79-96 PubMed.
  • Fenger C K, Granstrom D E, Langemeier J L & Stamper S (1997)Epizootic of equine protozoal myeloencephalitis on a farm.JAVMA210(7), 923-927 PubMed.
  • Sedrich S & Ramirez S (1996)What is your neurologic diagnosis? Equine protozoal myoeloenceohalitis.JAVMA209(5), 901-905 PubMed.

Other sources of information

  • 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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