Skip to content

Working on immunity to S neurona

horse-1399171__340

Not all species of Sarcocystis harm the intermediate host! Species passed by dogs are usually more damaging to the host than those transmissible by other definitive hosts and generally severity of signs depends on the dose of parasites. Horses don’t show any outward signs with initial S fayeri infections transmitted by dogs. Only a few horses show signs when they are infected with S neurona. S neurona infection is passed to the horse through opossums.

When a horse succumbs to S fayeri disease it takes a large dose of oocysts and usually in a debilitated animal. Infection can cause fever, anemia, and hair loss. Infected horses can have a stiff gait and muscle soreness. Experimentally it takes millions of oocysts to get clinical signs with S neurona. Microscopically, inflammatory cells are increased but not associated with parasites or the cysts found in muscles, inflammation is associated with host tissue cell death. New infections are most likely spread from the gut, re-exposure probably plays a large part in chronic inflammation for both Sarcocystis.

Little is known about chronic sarcocystosis (in the natural intermediate host) to explain the cause of central nervous system signs often seen in intermediate host infections. Some cysts may rupture from time to time releasing toxins. It has been known for 100 years that an extract of parasites (the bradyzoites) release a toxin. S fayeri infected horsemeat is toxic to humans, interestingly this is how the toxin was discovered and identified in Japan. A toxin wouldn’t be expected from S neurona infections in horses because this parasite doesn’t make muscle cysts. If it is discovered that neurona does make cysts in the horse, then the test for the fayeri toxin would be useful. Detection of neurona toxin using the fayeri assay is expected because the toxin is conserved in Sarcocystis and other cyst-forming pathogenic protozoa. Scientists haven’t identified S neurona cysts in horses, but they are looking again at tissues, this time with a fine-tooth comb. Our work shows no link (statistics used here) between horses with clinical signs and antibodies against S neurona and fayeri anti-toxin. One would expect a link if S neurona made a toxin.

Sarcocystis induce antibody production and the level of antibody (titer) increases with the duration of infection. Antibody may play a part in protection. It is cellular immunity that recruits white blood cells from tissues and the blood stream to fight and protect against parasites, including protozoa. Cellular immunity is evident 2 weeks after initial infection from oocysts. In certain animals Sarcocystis can depress immunity. Some proteins that are released during infection are cross-reactive with other Sarcocystis. When non-specific tests are used any cross-reactive antibodies will need to be diluted out (the reason the SAG 2, 4/3 starts at 250). In our lab we look for antibody made against the fayeri toxin released from cysts because we associate toxin with disease in susceptible horses. When we look for antibody against S neurona we use neurona specific proteins to identify serotypes (SAG 1, 5, 6).

Protective immunity is most likely associated with a sporozoite (found in the oocyst) or first-generation schizont. In some species sporocysts induce protective immunity that persisted for 80 days to 280 days. Protection can result from as little as 100 sporocysts. Protective immunity has only been shown with homologous (the same) species. We are working on the protocol to induce protective immunity in field exposure to Sarcocystis. It has been shown in mice and horses that ponazuril will decrease antibody production (detected by antibody assays) but not prevent signs of EPM.  In a mouse experiment mice were given drugs to prevent infections.  When the animals were removed from treatment and challenged, they succumbed to the disease.  Some protozoal vaccines have been attempted in pigs and mice.  Live, killed, or fractions of bradyzoites induced antibodies but provided no protection in these species.  The persistence of live sarcocysts is probably not crucial for maintaining protective immunity.  Goats are protected from challenge infection after initial infection from sporocysts.  We are working on it, stay tuned!