IN-DEPTH INTERACTIVE: NEUROLOGY


ratory testing, while also providing a brief review of tests for other infectious neurologic diseases.


General Approach


The majority of neurologic horses can be divided into those with brain disease, spinal cord disease, or multifocal CNS disease (neuropathies and neuro- muscular disease will not be discussed here).


● Brain disease: Adult horses develop brain disease most commonly due to metabolic, in- fectious, and traumatic causes. Recom- mended laboratory testing often includes serum biochemistry, blood ammonia level, CSF analysis (if available), and specific infec- tious disease testing (Table 1).


● Spinal cord disease: Adult horses develop spinal cord disease most commonly due to ver- tebral problems (developmental, degenerative, or traumatic) and infectious causes, al- though degenerative myelopathies also oc- cur. Recommended laboratory testing often includes CSF analysis (if available), vitamin E level, and specific infectious disease test- ing (Table 1).


● Multifocal CNS disease: Adult horses most commonly develop multifocal disease due to infectious causes. Recommended laboratory testing often includes CSF analysis (if avail- able) and specific infectious disease testing (Table 1).


Specific Diseases


EPM EPM is most commonly caused by the protozoan parasite Sarcocystis neurona, although infection with other protozoa such as Neospora hughesi has also been reported.1 Horses are infected by S. neu- rona when they consume food or water contami- nated with opossum feces containing sporocysts. The life cycle of N. hughesi is not well elucidated but vertical transmission likely plays a role.2 When these protozoa invade the central nervous system, they can affect any part, causing highly variable clinical signs that might manifest insidiously or sud- denly and subsequently progress slowly or rapidly. General proprioceptive ataxia is one of the most common clinical signs of disease, and is often asym- metric, with a mixture of upper and lower motor neuron paresis. Muscle atrophy (again, often asymmetric) is also common. Antemortem diagnosis of EPM remains challeng-


ing and is always presumptive; definitive diagnosis requires postmortem confirmation of protozoal infec- tion by microscopic identification, immunohisto- chemistry, culture, or PCR. Depending on geographic location, a high percentage of horses can be exposed to and infected by S. neurona, although only a small percentage of horses (estimated at1% of exposed horses) develop clinical signs of neuro-


198 2015  Vol. 61  AAEP PROCEEDINGS


logic disease. Factors that govern whether any particular horse is able to eliminate the infection without developing clinical signs are unknown. Therefore, performing serology, regardless of test cho- sen, will only reveal whether the horse has been ex- posed to S. neurona or N. hughesi and does not indicate the current disease status of the CNS. To achieve the best possible presumptive diagnosis in the live horse, three criteria must be met: presence of neurologic disease, exclusion of other likely causes, and confirmation of S. neurona– (or N. hughesi–) spe- cific antibodies in the CSF, serum, or both.3 All of the commonly used diagnostic tests for EPM


assess whether the horse has antibodies against the protozoa in serum, CSF, or both. The differences among the tests include their methodologies (West- ern blot [WB], indirect fluorescent antibody test [IFAT], or enzyme-linked immunosorbent assay [ELISA]) as well as which antibodies are recognized. A summary of commercially available testing op- tions for antibodies against S. neurona and reported test performance is shown in Table 2.4–17 There are two testing options for antibodies against N. hughesi: an IFAT at University of California at Davis and an ELISA at Equine Diagnostic Solu- tions.18–19 Neither has been fully evaluated using clinical EPM cases. General principles for interpretation of EPM test results are as follows:


● A positive serum test indicates exposure to the organism but does not confirm CNS infection, regardless of the magnitude of the titer.


● A negative serum test usually indicates that the horse has not been exposed to the organ- ism. Exception: rarely, a recently infected horse might show clinical signs prior to sero- conversion, in which case repeated testing in 10 to 14 days should yield a positive result.


● A positive CSF test is more likely to correlate with an EPM diagnosis than a positive serum test. However, false positives occur due to blood contamination (particularly with WB, less so with IFAT and ELISA) or normal diffu- sion of antibodies from blood to CSF.


● A negative CSF test usually means EPM is not the cause of disease. Exception: as men- tioned above, in rare circumstances a recently infected horse will show clinical signs prior to developing a measurable antibody level in CSF; retesting 10 to 14 days later should yield a positive result.


● The best way to diagnose active EPM is to submit serum and CSF for quantitative test- ing, which allows detection of intrathecal an- tibody production.16,20


The author’s current approach is to submit paired


CSF and blood samples for an S. neurona SAG2, 4/3 ELISA (or Neospora ELISA) serum:CSF titer ratio, which allows identification of intrathecal antibody


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