“A lie told often enough becomes the truth”. --Vladimir Lenin
If you’re not talking about inflammation, then-- by exclusion-- you’re lying about equine protozoal myeloencephalitis. Reviewing only the causative agents (protozoa), life-cycle of the parasite, antibody testing, and treatment perpetuates misunderstanding. Old ideas (EPM is enzootic and effectively untreatable, most horses are doomed to relapse) repeated often enough become a self-fulfilling prophesy.
Instead of viewing EPM as a population of horses infected with S. neurona containing a sub-group of untreatable, relapsing horses, chew on this. View the population of ataxic horses as the whole pie (data set). Ataxia is ubiquitous in horses and ataxia has several etiologies. Sometimes ataxia in horses is caused by S. neurona. Our data associates ataxia and S. neurona in 54% of ataxic horses.
The ideas are very similar, however the practical difference between the views is that we can treat the latter group successfully—we are all too familiar with the treatment success of the former group. Treating inflammation appropriately is key. Understanding and managing the two components of EPM, inflammation and infection, are important to long term success. The successful management of a horse with EPM will not be achieved by treatment alone, management takes an understanding the disease process. It takes some work and it isn’t hard.
We make the association based on a gait assessment score, GAS, and the presence of specific serum antibody to the predominant surface antigens of S. neurona-SAG 1, 5, or 6. A GAS of >1 and an ELISA SAG 1, 5, or 6 titer >8 attributes the ataxia to S. neurona. A response to treatment supports the diagnosis.
Horses that do not have antibodies to S. neurona, with a positive GAS, are considered the rest of the pie, 46%. Just for arguments sake, call this group of animals IE-- disease due to inflammatory encephalitis.
If licensed anti-protozoal drugs are used for treatment the treatment efficacy is (published) 58%. The difference in treating inflammation along with an anti-protozoal in suspect cases of EPM is 35%. Are we just treating IE horses with an effective immune modulator or is there reason to think S. neurona played a role in disease? That is an experimental question for scientists, horse owners and veterinarians want results.
When horses show signs after "EPM" treatment they are called “relapses”. Relapses are attributed to ineffective killing of anti-protozoals or re-infection. The relapse rate with conventional antiprotozoal drugs are reported as 25% (ReBalance) and 20% (Triazines)—all of these drugs decrease the detectable antibodies in serum leaving, on average, 17% of horses in the IE category—ataxic with no antibodies--these are post-treatment IE cases but are attributable to S. neurona. The rate of relapse (inflammation post-treatment) is three times higher in horses in which the inflammation was not addressed at the time of protozoal killing. Seventy one percent of ataxic horses with a presumptive diagnosis of EPM (no alternate diagnosis) had a root cause of inflammation that was most likely due to S. neurona infections. This should be the topic of conversation about EPM.
The math leaves us to believe that 22% of horses with IE are horses with inflammation with an undetermined cause. In some cases, we detect the effectiveness treatment for IE by serum CRP. The anticipated treatment failure rate of treating inflammation and ignoring the inciting infectious cause, including S. neurona, would be high. Our data indicates that S. neurona is a significant cause of IE in horses and should be a top consideration in treatment options. Our research indicates that inflammation is the larger issue. When treatment fails other obvious causes of IE should be investigated.