Abstract
Sarcocystis neurona, a parasite shed in the feces of the Virginia opossum (Didelphis virginiana), is an important cause of protozoal encephalitis among marine mammals of the central west coast of the United States and has been increasingly detected infecting marine mammals stranding along the northwestern United States and British Columbia coasts. This region, the Pacific Northwest, is home to a variety of marine mammals, including several endangered species, so understanding causes of mortality and potential impacts of pathogens at the land-sea interface is critical for this area. Samples from 142 stranded marine mammals were analyzed using a pan-apicomplexan primer set, ITS-1, in a nested PCR. All samples positive for S. neurona at the ITS-1 region were genotyped using molecular markers for 3 surface antigen genes, SnSAG1-5-6, SnSAG3, and SnSAG4.1 Based on polymorphic regions within these 3 surface antigen genes,2,3 this study identified a novel S. neurona genotype, called Type XIII, that was significantly correlated with an increased severity of protozoal encephalitis (P = 0.03) and mortality (P = 0.01) in nine stranded marine mammals singly infected with this protozoan parasite. Type XIII is genetically unrelated to the S. neurona Type I strain that caused a mass mortality epizootic in the threatened Southern sea otter (Enhydra lutris nereis) in 2004.3 Interestingly, however, the highly virulent Type I has only been documented in a single species.3 Here we identify Type XIII infecting both pinnipeds and cetaceans, thus indicating that this new S. neurona genotype is not only more virulent, but harbors the potential to infect multiple marine mammal species. Polyparasitism has previously been identified in the Pacific Northwest as an important factor associated with increased severity of protozoal encephalitis and associated mortality in marine mammals.4 Our study demonstrates the emergence of an additional genotypic variation of S. neurona infecting marine mammals of the Pacific Northwest and establishes parasite genotype as an essential factor mediating protozoal disease severity and related mortality in multiple marine mammal species.
Acknowledgements
The authors would like to thank staff and volunteers at the Washington Department of Fish and Game, and technologists with the Animal Health Center, Abbotsford, BC and with the Molecular Parasitology Unit at the National Institute of Allergy and Infectious Diseases. DNA sequencing was carried out by the Rocky Mountain Lab Genomic Unit DNA Sequencing Center, Division of Intramural Research, Hamilton, MO. This work was supported in part by the Intramural Research Program of the NIH and NIAID. MEG is a scholar of the Canadian Institute for Advanced Research (CIFAR) Program for Integrated Microbial Biodiversity.
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Literature Cited
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