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Title:   Author  item
                                            Dubey, Jitenderitem
                                            CHAPMAN, JENNIFER - WASHINGTON, DCitem
                                            Rosenthal, Benjaminitem
                                            MENSE, M - WASHINGTON, DCitem
                                            SCHUELER, RONALD - ELDERSBURG, MD
  Submitted to: Veterinary Parasitology
                                    Publication Type: Peer Reviewed Journal
                                    Publication Acceptance Date: 12/10/2005
                                    Publication  Date: 5/6/2006
                                    Citation: Dubey, J.P., Chapman, J.L., Rosenthal, B.M., Mense, M., Schueler, R.L. 2006. Clinical sarcocystis neurona, sarcocystis canis, toxoplasma gondii and neospora caninum infections in dogs. Veterinary Parasitology. 137:36-49.Interpretive Summary: Sarcocystis neurona is a single-celled parasite. It causes a fatal disease in horses called Equine Protozoal Myeloencephalitis (EPM). EPM also occurs in other animals. Opossums are the definitive host for this parasite, and the main reservoir of infection. Opossums become infected by consuming the encysted stage of the parasite (sarcocyst) in infected animal tissue and they excrete millions of the resistant stage (oocysts) in their feces. Horses become infected by ingesting food and water contaminated with oocysts.

Scientists at the Beltsville Agricultural Research Center  report  dfferential  diagnosis of S. neurona  infections in dogs for the first time. The results will be of interest to biologists, parasitologists, and veterinarians.
                                Technical Abstract: Sarcocystis neurona, Sarcocystis canis, Toxoplasma gondii, and Neospora caninum are related apicomplexans that can cause systemic illness in many species of animals, including dogs. We investigated one breeder's 25 Basset Hounds for these infections. In addition, tissues from dogs and other non-canine hosts previously reported as S. canis infections were studied retrospectively. Schizonts resembling those of S. neurona, and recognized by polyclonal rabbit anti-S. neurona antibodies, were found in six of eight retrospective cases, as well as in two additional dogs (one Basset Hound, one Springer Spaniel)  not previously reported. S. neurona schizonts were found in several tissues including the central nervous system, lungs, and kidneys. Fatal toxoplasmosis was diagnosed in an adult dog, and neosporosis was diagnosed in an adult and a pup related to the one diagnosed with S. neurona.  No serological reactivity to S. neurona antibodies occurred when S. canis-like liver schizonts were retrospectively assayed from two dogs, a dolphin, a sea lion, a horse, a chinchilla, a black or either of two polar bears. Sequencing conserved (18S) and variable (ITS-1) portions of nuclear ribosomal DNA isolated from the schizont-laden liver of a polar bear distinguished it from all previously characterized species of Sarcocystis. We take this genetic signature as provisionally representative of S. canis, an assumption that should be tested with future sequencing of similar liver infections in other mammalian hosts. These findings further extend the uncharacteristically broad intermediate host range for S. neurona, which also causes a neurologic disease in cats, mink, raccoons, skunks, Pacific harbor seals, ponies, zebras, lynxes, and sea otters.  Further work is necessary to delineate the causative agent(s) of other cases of canine sarcocystosis, and in particular to specify the attributes of S. canis, which corresponds morphologically to infections reported from wide range of terrestrial and marine mammals.


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