Necropsy reference number and summary collection information for Washington state population of northern sea otters examined during 1989-2010

• Main Authors: Thomas, Nancy, Knowles, Susan
• Format: Dataset
• Language: unknown
• Published: U.S. Geological Survey 2020
• Subjects: Wildlife Disease; Phoca vitulina; Alaska
• Online Access: https://dx.doi.org/10.5066/p90j7s7t; https://www.sciencebase.gov/catalog/item/5e9a092482ce172707f9320a

Morbillivirus epidemics in marine mammals first gained prominence in 1988 when an outbreak of phocine distemper virus (PDV) occurred in European harbor seals (Phoca vitulina vitulina). Prior to 2001, all serosurveys for morbilliviruses in sea otters (Enhydra lutris) in California, Washington and Alaska documented a 0% seroprevalence. The first published serodetections of morbillivirus in sea otters occurred in 2001?2002 in live-captured Washington sea otters with a documented 80% seroprevalence. We conducted a retrospective study of sea otter cases from 1989?2010 compiled at the U.S. Geological Survey?s National Wildlife Health Center to identify cases of morbilliviral disease in Washington sea otters, and to characterize the disease using immunohistochemistry, RT-PCR, genetic sequencing, virus isolation and serology. We identified six cases of morbilliviral disease and 12 of morbilliviral infection in this population of sea otters during 2000?2010. Significant histologic findings included inflammation in the white and gray matter of the brain characterized by lymphoplasmacytic perivascular cuffing, neuronal necrosis and satellitosis in gray matter and spongiosis, myelin degeneration, spheroids, and gemistocytes in white matter. Intranuclear and intracytoplasmic viral inclusion bodies were found in neurons, Purkinje cells and glia. Immunohistochemistry for canine distemper virus (CDV) showed positive staining in neurons, glial cells and cell processes. A pan-morbillivirus RT-PCR with subsequent restriction endonuclease digestion or sequencing identified canine distemper virus. Virus isolation was not successful. Two otters with morbilliviral encephalitis showed greater antibody titers to CDV than PDV. Histologic changes were confined to the central nervous system and resembled neurologic canine distemper in domestic dogs. Cases of otters with morbilliviral infection without histologic changes could represent early infections or incompletely cleared sublethal infections. Our findings indicate that morbillivirus was present in the Washington sea otter population as early as 2000 and provides a description of the pathology of canine distemper in sea otters.