How many horses die from EPM? It’s a complicated answer.
A complicating factor is that horses can have neuroinflammation that is not due to EPM. A horse that has neuroinflammation is wobbly. They have an unexplained lameness, and…well, looks just like a horse with EPM! And that is because EPM is a sub-set of these horses—they are EPM horses when we know S. neurona is the cause of the neuroinflammation. If we don’t know the cause then they are idiopathic, we call them idiopathic encephalomyelitis or IE.
How many horses have signs that look like EPM but are unrelated to S. neurona infections? We looked at sera from 4298 horses that had signs of EPM that were not treated with antiprotozoal drugs and found that 55% were seronegative to S. neurona. It’s important to point out that antiprotozoal drugs can alter the detection of S. neurona antibodies (Martin Furr published data to show that treating horses with Marquis delayed antibody production without altering the development of disease).
Exposure to antiprotozoal drugs is probably not the reason that the majority of the sera we tested were seronegative. We are aware that 20% of seronegative EPM suspect horses will show a rise in antibody titer shortly after treatment. Seroconversion takes place about 17 days after infection, faster in an “experienced” (has been infected before) animal and a bit slower in a “naive” (never had an S. neurona infection) animal. That is why it is important to test for serum antibodies against S. neurona 10 days after the end of treatment. Seroconversion supports the diagnosis of EPM.
Generally, 55% of animals being treated for EPM by veterinarians (suspect EPM due to ataxia and not tested) would be treating the wrong disease. If the treatment was only an anti-protozoal then the disease isn’t being treated. Could another serum test help identify the horses on the wrong treatment path?
A retrospective analysis of data obtained from serum C-reactive protein (CRP) concentration (from 1424 sera from animals with neuroinflammation tested for before any treatment was initiated) was divided into groups: those with S. neurona antibodies (supporting the diagnosis of EPM) and those that were seronegative (supporting a diagnosis of idiopathic encephalomyelitis). The purpose of the analysis was to examine serum CRP levels from horses that died, presumably due to EPM, perhaps identifying CRP as predictor of survivability for EPM. Sixty seven horses died. That means 5% of horses that were tested for EPM died before treatment.
The group of horses that succumbed to disease in this analysis died for various reasons and not all were treated (or treated with an anti-protozoal) therefore an analysis by treatment was not possible.
The results of the query indicated that 35% of the dead horses had a high serum CRP concentration (before treatment) in the EPM group while 61% of the horses that died had a high serum CRP concentration (before treatment) in the IE group.
Serum CRP is an indicator of non-specific inflammation due to bacteria, virus, and protozoa. The CRP value falls when the inciting cause of inflammation resolves with proper treatment. These data may indicate that a significant number of horses with suspect EPM actually have another etiology. Anti-protozoal agents are highly specific for pathogenic protozoa. The change in CRP, before and after treatment, may be useful in determining resolution of the infection. When the CRP remains elevated it’s time to look alternate causes of ataxia.
The original question was “How many horses die from EPM”? Retrospective analysis of our database indicated death in suspect EPM (seropositive for S. neurona) horses is 1.3% of cases. These horses have a history of multiple antiprotozoal treatments with diminishing returns.
How about idiopathic encephalomyelitis? We have the data to answer that question. Death in horses with IE (seronegative for S. neurona) that had a history of treatment with an antiprotozoal agent is 25%. The death rate may be high because alternate causes of disease are not considered.
A definitive diagnosis for EPM remains elusive and a response to treatment is a logical approach. However, when there is no response to treatment the diagnosis is idiopathic encephalomyelitis and working up the case is important. C-reactive protein may be a parameter to monitor response to treatment when the diagnosis remains open.