Equine Protozoal Myeloencephalitis Flashcards

1
Q

What causes equine protozoal myeloencephalitis? What is the definitive host? How do horses play into the life cycle?

A

Sarcocystis neurona

opossum

horses are aberrant (dead-end) hosts

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2
Q

What is the lifecycle of Sarcocystis neurona like? How do horses play into is?

A
  • opossum releases infective sporocysts into the food and water of IH (prey) hosts
  • upon ingestion by the IH, sporocysts excyst and eventually enter skeletal muscle cells where they develop into sarcocysts
  • life cycle is completed when the DH ingests the sarcosysts within the muscle of the IH

the horse is an aberrant (dead-end) host the ingests sporocysts

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3
Q

What are the classical clinical signs associated with EPM? What are some other less common signs?

A

affected horse is bright and alert, but demonstrates ASSYMETRIC ATAXIA, weakness, and muscle ATROPHY (3 A’s)

  • head tilt
  • facial paralysis
  • masseter muscle atrophy (brainstem involvement)
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4
Q

What is the distinguishable feature of EPM when compared to cervical vertebral malformation?

A

asymmetry associated with EPM

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5
Q

What are some supportive diagnostics for cases of EPM?

A
  • positive Western blot analysis of CSF for S. neurona
  • immunofluorescent antibody testing

(mostly by clinical signs –> asymmetry, ataxia, atrophy)

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6
Q

What are the 3 primary treatments for EPM?

A
  1. Trimethoprim-sulfonamide and pyrimethamine - blocks folate metabolism is protozoa
  2. Ponazuril - anti-protozoal that targets plastid (organelle)
  3. Nitazoxinade - inhibits electron transfer reactions essential for energy metabolism
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7
Q

What is prognosis for equine protozoal myeloencephalitis like?

A

variable - some horses completely recover while others may have little to no improvement or have residual neurologic deficits

  • neurologic signs may persist
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