S. Raverty1; S. Etheridge1; M.B. Hanson2; S. Norman3; J. Calambokidis4; J. Huggins4; J. Ford5; E.James6; M. Grigg7
Abstract
Over the course of the last 7 years, there have been increasing efforts within the Pacific Northwest to recover dead, beach-caste marine mammals. Between January 1, 1999 and December 31, 2006, there were 132 stranded small cetaceans documented, including 90 harbor porpoises (Phocoena phocoena), 19 Dall's porpoises (Phocoenoides dalli), 15 Pacific white-sided dolphins (Lagenorhynchus obliquidens), 2 short-beaked common dolphins (Delphinus delphis), 1 northern right whale dolphin (Lissodelphis borealis), 1 bottlenose dolphin (Tursiops truncatus), and 4 unidentified animals. A proximate cause of death could be determined in approximately 40-60% of examined animals and general diagnostic categories include infectious, trauma, emaciation, and possible metabolic derangements.
In 2006, two independent strandings expanded the list of recognized pathogens of small cetacea within the Pacific Northwest. An adult, 172 cm total length, moderately emaciated female Pacific white-sided dolphin recovered January 19, 2006 from Grayland, Washington State and an adult, 144 cm total length male harbor porpoise obtained from Bellingham Bay, (48°45.816 N, 122°30.900 W) September 14, 2006. Field necropsies were undertaken for both animals and aside from post mortem scavenging, there were no significant gross observations.
Microscopic examination of the Pacific white-sided dolphin revealed a marked nonsuppurative and necrotizing meningoencephalitis with perivascular lymphoplasmacytic cuffing, scattered gliosis and intralesional protozoal schizonts and dispersed merozoites. Verminous gastritis, splenic lymphoid hyperplasia, and mild interstitial pneumonia were also noted. In contrast, the harbor porpoise presented with a moderate interstitial pneumonia, peribronchial lymphofollicular hyperplasia and florid predominantly intravascular accumulations of protozoa, mild nonsuppurative encephalitis, cholangiohepatitis, myocarditis, and tonsillitis. In both cases, immunohistochemistry was strongly positive for Sarcocystis neurona. In the dolphin, there was a weak staining for Toxoplasma gondii and in both animals, tissues were negative for Neospora caninum. Preliminary genotyping confirmed Sarcocystis spp with concurrent Toxoplasma gondii in the dolphin and additional molecular characterization is underway.
Sarcocystosis due to S. neurona has been implicated as a contributory factor in the decline of sea otters (Enhydra lutris) from California to Washington State and more recent work has detected fatal infections in harbor seals (Phoca vitulina) within the Northeast Pacific. These porpoise and dolphin cases are believed to be the first reports of sarcocystosis due to S. neurona in small cetaceans. The epizootiology and pathology of this infection is currently unknown; however, based on extrapolation from pinniped and otariid infections, it is possible that this pathogen may contribute to morbidity and possible mortalities in these populations.