Neuroinflammation

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The idea that EPM is primarily an immune mediated disease, perhaps obvious, is not readily accepted.  Parasites were isolated from brain tissue in experimentally infected horses (Ellison.  Intern. J. App. Res. Vet Med. 2004. p 79-89).  In this experiment, immuno-affinity beads were used to trap parasites from large volumes of neurological tissues—a technique that was key to proving the success of this model.  A highly virulent strain of S. neurona was employed in these studies. The organism was passed through a horse (with re-isolation) to increase the organisms virulence for horses.  Passing the organism through other species (such as a raccoon) result in parasites that are less virulent for horses.

The evidence that parasites (S. neurona) are associated with brain lesions is lacking in the majority of clinically diseased animals as well as experimentally infected horses (Saville. Vet Parasitol. 2001. Feb; p 211-22). What was clearly demonstrated in the Saville model is that clinical signs are associated with inflammation—not protozoa. Therefore it is generally accepted that clinical signs (neuroinflammation) and the presence of S. neurona antibodies define a horse with EPM pre-mortem. Even post-mortem diagnosis of EPM does not depend on demonstration of the protozoa (Saville).

Treating a horse with antiprotozoal drugs for EPM can result in elimination of antibodies and, in some cases, incomplete resolution of clinical signs.  Treating specific neuroinflammation can result in resolution of disease in these horses.  There are several inflammatory molecules that play a role in the modulation of the early immune response  to parasitic protozoa.  Molecules and their receptors are active areas of research.

We found data from a recent paper showing levels of specific neuroinflammatory molecules (found in brain and blood) distinguished between treated animals that had cleared systemic parasites, but not those in the brain, interesting.  It will take years of research to apply these tests to horses with EPM, should researchers even take on the work.  The first step in investigating the inflammatory component of EPM is recognizing the importance of neuroinflammation in disease. However, these tests may be instrumental in accruing more evidence that the vast majority of horses with EPM don’t have active parasites in the CNS.  Certainly the outcome will change the approach to treating EPM.

 

 

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