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Title:   Author  item
                                            Dubey, Jitenderitem
                                            ROSYPAL, A - VIRGINIA TECHitem
                                            Rosenthal, Benjaminitem
                                            THOMAS, N - NAT'L WILDLIFE HEAL. CTR.item
                                            LINDSAY, D - VIRGINIA TECHitem
                                            STANEK, J - OHIO STATE UNIVERSITYitem
                                            REED, S - OHIO STATE UNIVERSITYitem
                                            SAVILLE, W. - OHIO STATE UNIVERSITY
  Submitted to: Journal of Parasitology
                                    Publication Type: Peer Reviewed Journal
                                    Publication Acceptance Date: 12/28/2001
                                    Publication  Date: N/A
                                    Citation: N/AInterpretive Summary: Sarcocystis neurona is a single-celled parasite of horses and it causes a fatal disease, equine protozoal myeloencephalitis (EPM) in horses in America.  It also causes a fatal neurologic disease in sea otter and other sea mammals.  Its complete life cycle is unknown.  Opossums are its reservoir hosts and excrete a resistant-stage in their feces.  How opossums sbecome infected with the parasite is not fully known.  Scientists at the Beltsville Agricultural Research Center and the Ohio State University have found that sea otter is a natural host for this parasite and opossums can become infected by eating tissues of infected sea otters.  These results will be of interest to parasitologists, biologists and horse owners.
                                Technical Abstract: Although Sarcocystis neurona has been identified in an array of terrestrial vertebrates, recent recognition of its capacity to infect marine mammals was unexpected.  Here, sarcocysts from 2 naturally infected sea otters, Enhydra lutus neries, were characterized biologically, ultrastructurally, and genetically.  DNA was extracted from frozen muscle of the first of  these sea otters, and characterized as S. neurona by PCR amplification followed by restriction fragment length polymorphism analysis and sequencing.  Sarcocysts from sea otter No. 1 were up to 350 mm long and the villar protrusions on the sarcocyst wall were up to 1.3 mm long and up to 0.25 mm wide.  The villar protrusions were tapered towards the villar tip. Ultrastructurally, sarcocysts were similar to S. neurona sarcocysts from the muscles of cats experimentally-infected with S. neurona sporocysts. Skeletal muscles from a second sea otter failed to support PCR  amplification of markers considered diagnostic for S. neurona, but did induce the shedding of sporocysts when fed to a laboratory-raised opossum (Didelphis virginiana).  Such sporocysts were subsequently fed to interferon-gamma gene knockout mice, resulting in infections diagnosed as Sarcocystis neurona on the basis of immunohistochemistry, serum antibodies, and diagnostic sequence detection.  Thus, sea otters are exposed to S. neurona infections and may support the development of mature sarcocysts which are infectious to competent definitive hosts.


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