Sarcocystis neurona is primarily a neural parasite of horses and its management is of concern in veterinarian medicine. The protozoan Sarcocystis neurona is a protozoan of single celled character and belongs to the family, Sarcocystidae, a group called coccidia. The protozoan, S. neurona, is a member of the genus Sarcocystis, and is most commonly associated with equine protozoal myeloencephalitis (EPM). The protozoan, S. neurona, can be easily cultivated and genetically manipulated, hence its common use as a model to study numerous aspects of cell biology.
Life cycle
Sarcocystis neurona has a wide range of potential intermediate hosts, making it one of the most unique life cycle of the genus Sarcocystis. The life cycle of this parasite requires two hosts, a definitive and an intermediate host. The definitive host of S. neurona are opossums, and more specifically opossums of species Didelphis virginiana and D. albiventris. The full life cycle of S. neurona has yet to be understood, but many advances have been made in fully understanding it after the publication of this subject in 2001 by Dubey. Environmentally resistant oocysts and sporocysts are released into the environment by the definitive hosts (opossums) feces. Numerous mammals primarily including armadillos, raccoons, sea otters, skunks, and cats serve as intermediate hosts for S. neurona and ingest many sporocysts. After multiple asexual cycles, the sporocysts develop into a resting stage in their muscles called sarcocysts. The sarcocysts produced from the muscles of the intermediate host are ingested by the definitive host and bradyzoites are released in the intestine of the definitive host. The bradyzoites result in sporulated oocysts by undergoing a sexual cycle. The sporulated oocysts are excreted in the feces of the opossum. Horses are aberrant or dead-end hosts, because only schizonts and merozoites have been identified and confined to the brain in spinal cord after a horse has ingested sporocysts in contaminated water and feed. This disease cannot be passed from horse to horse.
Pathogenesis
There are many unanswered questions concerning the development of the disease once this protozoan infects the horse by ingestion of sporocysts in contaminated water and feed. It is presumed that sporocysts release sporozoites that are able to penetrate the intestinal wall and enter arterial endothelial cells within the horse. It is assumed that schizonts develop in these cells until the cell ruptures and merozoites are released into the bloodstream, repeating this stage numerous times to produce large numbers of merozoites. During this stage, no clinical signs or the protozoan can progress to the central nervous system, but the infection can be cleared leading to seropositivity. How S. neurona enters the central nervous system of horses is unknown, but it has been hypothesized that merozoites enter the central nervous system through cytoplasm of endothelial cells or by infected leukocytes. When the merozoite accesses the central nervous system, it is suggested that schizonts form in one or more areas of the CNS including the cerebrum, brainstem, cranial nerves, and/or the spinal cord of the horse. Transmission of the protozoan from the infected horse to other animals is not possible based on the schizonts and daughter merozoites remaining uninfective in the neural tissue. Recent studies suggest that approximately 22-65% horses in the United States, depending on the geographic location, are seropositive for S. neurona antibodies. Although theories are often developed, the reason explaining why only some horses develop clinical signs of S. neurona and some do not is unknown. Theoretical factors including stress and further unrelated health events are thought to contribute to the onset of this disease. Little is known about the incubation period between exposure to the protozoan and development of clinical disease of Sarcocystis neurona.