EPM Flashcards
What is the primary causative agent of equine protozoal myeloencephalitis (EPM)?
Sarcocystis neurona
-can also be caused by neospora hughesi (much less common)
Describe the life cycle of sarcocystis neurona
2 host life-cycle
-definitive host is the opossum (where sexual development of organism occurs)- sporocysts are passed into the environment
-sporocysts are consumed by intermediate hosts to include skunks, raccoons, cats, sea otters, armadillos- sarcocysts form in skeletal muscle
- opposums are reinfected when they consume the meat of intermediate hosts
Can horses get EPM from cats?
No- they would have to ingest cat meat for this to be possible
How do horses get EPM?
From ingestion of sporocysts in environment
- they are aberrant dead end hosts
Describe the prevalence of EPM
-it is a naturally occurring disease in north and south America
-testing indicates widespread exposure (40-60% blood positive)
-less than 1% of horses develop disease (dose related, strain difference or to due with individuals immune response)
What are some individual factors that can contribute to the development of EPM?
Stress, Season, Location, Age, Other diseases, pregnancy
* decreased immune response is correlated to disease
What clinical signs result from infection with EPM?
It is completely dependent on the part of the CNS affected
-can be multifocal or focal (this is the top differential for multifocal CNS disease in horses)
-most commonly results in ataxia, asymmetry, and atrophy
-it is usually slowly progressive (but occasionally can be severe and acute)
How is EPM diagnosed?
-confirm the presence of clinical signs that are consistent with EPM through performing a complete neurological exam and/or lameness exam
-rule out other diseases (with lameness exam, CBC/chem, serology, radigraphs/myelogram, cerebrospinal fluid cytology)
-confirm intrathecal antibody production through immunodiagnostic testing on serum and CSF
What are the common hematology and serum biochemistry results with EPM? What about CSF cytology?
All of these are usually normal- doesnt affect any other organ system
- however, CSF can be used to test for S neurona antibodies
- abnormal cytology does not rule out EPM (but makes other diseases more likely
What options do you have in terms of tests on the CSF to confirm intrathecal antibody production?
-Western blot - not done much anymore
- ELISAs (SAGs), serum to CSF ratio
-IFAT
Why is serum testing alone unreliable in EPM cases?
A lot of horses are positive, but few actually show signs of disease
- a serum antibody titer for S neurona does not mean the horse has active EPM
-very high prevalence of exposure with very low prevalence of clinical disease= low positive predictive value
*negative predictive value is high however - can trust a negative test (unless in early disease- retest in 10-14 days)
What is the best way to diagnose horses with EPM?
- testing of CSF (often referral)
-specifically comparing CSF to serum levels
What is the problem with just testing CSF?
High titer levels in the blood may spill over to CSF past the BBB even without clinical disease
Describe the problem with the IFAT (Immunoflourescent antibody test)
- little correlation with active infection
- does not take into account that antibody level is dependent on that individual animals immune system (or amount/chronicity of exposure)
- better results when you send off both blood and CSF
Describe the SAG ELISA
- SAG- surface antigens produced by Sarcoptes
- more likely to be expressed when animal has active disease
SAG 1- not all pathogenic S neurona isolates express this antigen (low sensitivity)
SAG 1, 5, 6 - very little published evidence
SAG 2, 4, 3 - shown to be the most consistently expressed antigens across isolates (still test both serum and CSF)
