The abstract outlines the purpose of the study “to determine if the (previously developed killed) vaccine could prevent development of clinical signs after challenge with Sarcocystis neurona sporocysts in an equine challenge model”.
Seventy horses were selected because they were negative for antibodies to Sarcocystis neurona and neurologically normal. These horses were divided into not vaccinated (placebo), vaccinated twice (short term immunity), or vaccinated three times (long term immunity). In this study, all horses developed neurological signs and there was no difference between the vaccinates and controls. They reported that neurologic signs were worse in the vaccinated horses when compared to the control, unvaccinated horses.
You have to get your hands on a copy of the complete manuscript to realize this paper reports the study conducted from September 2003 through May of 2004. This paper reports the laboratory testing of the old Fort Dodge EPM vaccine that was discontinued! Before you walk away, there are a few things of note in the paper.
They used 1.5 million sporocysts to induce disease. That’s a huge number. It is important to realize the difference between the study dose and the dose a horse will most likely ingest in a field situation. The type and degree of inflammation that is induced in the overwhelming lab dose, compared to chronic inflammation induced under field conditions, are different. Chronic, low dose exposure most likely induces sub-clinical inflammation (inflammation that won’t be detected clinically for awhile). The result of chronic inflammation may be polyneuritis. If you have questions, read our blogs about detecting polyneuritis in horses.
The 2017 paper reports that some horses did not seroconvert against S. neurona. Nor did some develop antibodies to S. neurona in the CSF. These horses had clinical signs and were “false negative”. This is new evidence to suggest that high doses of parasite challenge, in addition to previously recognized cases in which low parasite challenge does not result in antibodies in the CSF, can be reported as false negatives. When the test was modified so that the test antigen was identical to the challenge antigen, antibodies were detected. It is a fault of the test design to detect antibodies, not a function of absent immune response in the horse.
The far reaching implications relate to S. falcatula challenge studies conducted at UF in which horses did not produce antibodies (serum or CSF) when tested against a S. neurona (SAG 1 strain) by western blot. The S. falcatula study concluded that horses can’t be infected with S. falcatula. Is this true or a fault in test design? Remember that S. falcatula and S. neurona share the SAG 6 serotype antigen. The inability to produce disease and share antigens could relate to field protection, or not.
The authors of the 2017 paper reiterate that “S. neurona strain differences and antigen preparation in the assay appear to make a difference. There is a lack of correlation between assay methods such as agglutination titers, IFAT, and western blot reactivity”.
Because the authors state they are not aware of any S. neurona vaccine trials in horses, let me direct you to our home page http://pathogenes.com/w/ . In 2009 we published (and presented to the EPM society after publication) a 10 horse, placebo controlled, blinded study in which a recombinant vaccine protected against S. neurona SAG 1 in an equine challenge model. We also provided evidence that a rSAG1 vaccine will not protect against a SAG 5 strain unless the horse has been exposed to a SAG 5 strain. This means a vaccine will have to be multivalent. We provided evidence that acute disease and chronic (disease greater than 30 days) were different.
We have a prevention strategy that is based on multiple S. neurona phenotypes and serotypes. If you have questions you may contact us though the web page contact information.