THE LESSER KNOWN PAR­A­SITE

EQUUS - - Epm -

Although Sar­co­cys­tis neu­rona is the most com­mon cause of equine pro­to­zoal myeloen­cephali­tis (EPM) in Amer­i­can horses, a dif­fer­ent pro­to­zoal or­gan­ism,o Neospora hugh­esi,h is re­spon­si­blere­spon­sib for a smaller but sig­nif­i­cant num num­ber of cases.

The life cy cy­cle of N. hugh­esi is not well un­derst un­der­stood, but it ap­pear ap­pears that horses canc be­come in­fec in­fected with­out consu con­sum­ing con­tam­i­nated feed or wa­ter—a top­icto Ni­cola Pu Pusterla, DVM DVM, PhD, DACVIM,DA hash been in­ves­ti­gat­ing at the Uni­ver­sity of Cal­i­for­nia– Davis. “A closely re­lated or­gan­ism called Neospora can­inum causes abor­tion in cat­tle and has a huge eco­nomic im­pact on the live­stock in­dus­try,” he says. “In cat­tle there are two routes of trans­mis­sion. One is hor­i­zon­tal—go­ing to cat­tle from the de­fin­i­tive host [dogs or wild ca­nines, who pass the oocysts in their fe­ces]. But the most ef­fi­cient way the or­gan­ism is trans­mit­ted in cat­tle is ver­ti­cally, from an in­fected dam to the off­spring dur­ing ges­ta­tion.” N. can­inum re­pro­duces in the cow’s in­tes­tine, then passes from the blood­stream through the pla­centa into the fe­tus.

“There can be dif­fer­ent out­comes, depend­ing on the stage of ges­ta­tion when the fe­tus is ex­posed,” Pusterla says. “In­fec­tion of the fe­tus can cause abor­tion, still­birth or birth of a per­sis­tently in­fected an­i­mal, depend­ing on the im­mune stage of the fe­tus when in­fec­tion oc­curs.” If a fe­male calf is born with the in­fec­tion, she in turn can pass the par­a­site on to her own off­spring when she ma­tures.

“About 95 per­cent of the in­fec­tions in cat­tle oc­cur ver­ti­cally—from dam to fe­tus—and this mode of trans­mis­sion also oc­curs in horses,” says Pusterla. “I worked with a herd that had two mares who tested sero­log­i­cally pos­i­tive to Neospora hugh­esi. Ev­ery one of their off­spring that we tested showed ev­i­dence of ver­ti­cal trans­mis­sion. All their foals were healthy but had ev­i­dence of transpla­cen­tal trans­mis­sion; they were born with high an­ti­body lev­els to N. hugh­esi be­fore they even in­gested colostrum. This is a very ef­fec­tive way for this or­gan­ism to be re­tained in horse pop­u­la­tions.”

This find­ing has se­ri­ous im­pli­ca­tions for the po­ten­tial range of EPM as horses are moved about the coun­try. “When re­ports about N. hugh­esi first came out in the mid-1980s, it was thought that this par­a­site oc­curred only on the West Coast,”

says Pusterla. “But we found that this or­gan­ism is more wide­spread, based on sero­log­i­cal data from a few years ago. That data showed that there were seropos­i­tive an­i­mals with high an­ti­body titers to N. hugh­esi in horses from about 25 states. In­fec­tion with N. hugh­esi could be found in horses any­where.”

That means that EPM is a pos­si­ble di­ag­no­sis for horses with neu­ro­log­i­cal signs even if they live in re­gions where S. neu­rona typ­i­cally isn’t found. “S. neu­rona iss present only in ar­eas where the de­fin­i­tive host is present, which is the opos­sum,” says Pusterla. “The far­ther north you go, the e less fre­quently we find opos­sums or EPM.” How­ever, he adds, “N. hugh­esi is wide­spread ad across the U.S. and it is a pathogen that is prob­a­bly spread far­ther than S. neu­rona.”

Nev­er­the­less, says Amy John­son, DVM, DACVIM, of the Uni­ver­sity of Penn­syl­va­nia, at least for now, the pre­pon­der­ance of EPM cases oc­cur only in cer­tain re­gions: “The West­ern states see far more clin­i­cal cases of N. hugh­esi than we do here on the East Coast. It has been found nearly ev­ery­where in the United States, but in terms of a causative agent it is not as com­mon here. In the seven years I’ve been here at the New Bolton Cen­ter I’ve seen only three N. hugh­esi cases, com­pared to well over a hun­dred caused by Sar­co­cys­tis. So there are some re­gional dif­fer­ences.” horses who de­velop EPM, and par­tic­u­larly the horses who de­velop re­cur­rent in­fec­tions. Now and then we get a horse who re­sponds to treat­ment but then has a sub­stan­tial re­lapse or fre­quent re­lapses.”

An­other pos­si­bil­ity is that some strains of th­ese par­a­sites are more vir­u­lent than oth­ers. “Siob­han El­li­son [DVM, PhD], in Florida, pre­sented her hy­poth­e­sis that cer­tain pro­to­zoa have sur­face anti­gens that might be more likely to be in­fec­tious,” Reed says. “This is cer­tainly a pos­si­bil­ity.”

Ad­vances in di­ag­nos­tics and treat­ments have come a long way to­ward re­duc­ing the num­ber of horses who suc­cumb to EPM. Find­ing more ef­fec­tive ways to pre­vent and treat this dis­ease is a chal­leng­ing goal---but one that re­searchers have real hopes of achiev­ing in the years to come.

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