Neospora hughesi is an obligate protozoan apicomplexan parasite that causes myelitis and equine protozoal myeloencephalitis (EPM) in horses, and has only been documented in North America.

(including N. caninum), and Toxoplasma gondii until the 1970s, when innovations in macromolecular analysis suggested phenotypic and molecular differences, which resulted in the divergence of species.

[4] Neospora hughesi is named after one of the discoverers, J.P. Hughes, a veterinary researcher whose interests in toxoplasmosis, sarcocystosis, and neosporosis, led to the differentiation of the aforementioned species.

[1] Via transmission electron microscopy (TEM) of parasites isolated from equine spinal cord tissue, E. Marsh et al. discovered a distinct species, Neospora hughesi.

[1] Tachyzoite pellets and the control cells were separated via SDS-PAGE, and purified antigens were transferred to nitrocellulose gel incubated with antibodies to determine molecular characterization via Polymerase Chain Reaction (PCR).

[1] In the definitive host (which is unknown at this time), the parasite undergoes its proliferative cycle in the intestines, ultimately passing unsporulated oocysts (sporozoites) in feces.

[8] These oocysts then sporulate from the fecal matter, and when an intermediate host (the horse) ingests them, tachyzoites proliferate and form cellular conglomerates composed of bradyzoites (quiescent cells) in both skeletal and nervous tissues (including the spinal cord).

[8] Tachyzoites in the intermediate host (horses) vary in shape from crescent-shaped to round and measure around 7μm by 5μm, and are found in a variety of organs and tissues.

[8] The organisms classified under the Apicomplexa phylum possess a unique organelle structure called an apicoplast, which plays a vital role in lipid metabolism.

[9] The apicoplast genome is comparably small, with a size of 35 kb encoding 30-50 genes which are involved in fundamental cellular processing utilizing DNA and RNA.

The largest partial apicoplast genome sequenced is a 440bp linear DNA that encodes for the RNA polymerase beta subunit gene.

Transmission from N. hughesi-infected horses to foals has been reported, but not all will develop clinical disease, as is supported in N. caninum studies in canines and coyotes.

[13] With the increased transportation of horses from the United States to other countries, it is critical that more research be conducted to understand the mechanisms and definitive hosts to prevent the spread of N. hughesi before it becomes transmissible in other parts of the world.