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Postmortem data for harbor seals (Phoca vitulina richardsii) in the Salish Sea were analyzed for epidemiologic trends in congenital diseases. Cleft palate, cleft lips, or both (n=8) and cardiac defects (n=5) were the most common congenital abnormalities, followed by cases with multiple defects (n=4). No temporal trends or spatial clusters of cases were seen from 2003 to 2019, during which time monitoring effort was consistent. Cases could not be linked to specific causes such as environmental contamination or maternal malnutrition. Our study suggests that a yearly prevalence of 2.9%±2.2 is the endemic level of congenital disease in this stable harbor seal population. Continued monitoring of birth defects and overall harbor seal population status could help to identify emerging teratogens., (© Wildlife Disease Association 2021.)

Documenting human impacts on marine mammals is critical for understanding and mitigating harm. Although propeller strike injuries in small marine mammals are often debilitating and fatal, little is known about the occurrence or demographics of these types of injuries in pinniped populations. Using data of stranded harbor seals (Phoca vitulina) in the Salish Sea from 2002-19, we identified 27 cases of fatal propeller strikes. Weaned pups were the most frequently affected (64% of cases) with a much higher rate of propeller strikes than expected for the age class. Although they do represent animal welfare concerns, harbor seals in the Salish Sea probably are not threatened by these types of injuries at the population level; nevertheless, propeller strike cases increased significantly over the time of this study period, indicating increased interactions between boats and seals in the region. Continued monitoring and increased efforts to consistently quantify vessel traffic in the area are recommended to create and monitor long-term effectiveness of mitigation measures., (© Wildlife Disease Association 2021.)

In 1994 a novel Brucella sp., later named B. pinnipedialis, was identified in stranded harbor seals (Phoca vitulina). This Brucella sp. is a potential zoonotic pathogen and is capable of causing disease in domestic animals. Serologic, microbiologic, and pathologic data collected from live captured and stranded harbor seals were used to better describe the epizootiology of B. pinnipedialis in harbor seals from Washington State, USA, in 1994 through 2006. We found no sex predilection in harbor seal exposure or infection with B. pinnipedialis but noted a significant difference in prevalence among age classes, with weaned pups, yearlings, and subadults having highest exposure and infection. The most common postmortem finding in 26 Brucella-positive animals (culture and/or PCR) was verminous pneumonia due to Parafilaroides spp. or Otostrongulus circumlitus. Our data are consistent with exposure to B. pinnipedialis post-weaning, and it is likely that fish or invertebrates and possibly lungworms are involved in the transmission to harbor seals. Brucella pinnipedialis was cultured or detected by PCR from seal salivary gland, lung, urinary bladder, and feces, suggesting that wildlife professionals working with live, infected seals could be exposed to the bacterium via exposure to oral secretions, urine, or feces. Endangered sympatric wildlife species could be exposed to B. pinnipedialis via predation on infected seals or through a common marine fish or invertebrate prey item involved in its transmission. More work is required to elucidate further potential fish or invertebrates that could be involved in the transmission of B. pinnipedialis to harbor seals and better understand the potential risk they could pose to humans or sympatric endangered species who also consume these prey items.

Tissue perforation and penetration by dorsal fin spines of spotted ratfish (Hydrolagus colliei) were responsible for the death of seven harbor seals (Phoca vitulina) in Washington State (USA) between 2006 and 2011. In six animals, necropsy revealed spines or spine parts that had perforated the esophagus or stomach and migrated into vital tissues, resulting in hemothorax, pneumothorax, pleuritis, and peritonitis. In a seventh case, a ratfish spine was recovered from the mouth of a harbor seal euthanized due to clinical symptoms of encephalitis. Gross examination revealed an abscess within the left cerebrum, which was attributed to direct extension of inflammatory infiltrate associated with the ratfish spine. Between 2009 and 2011, spotted ratfish spines were also recovered from the head or neck region of three Steller sea lions (Eumetopias jubatus) and one California sea lion (Zalophus californianus). Ratfish-related trauma appears to be a novel mortality factor for harbor seals in Washington State and could be related to increased ratfish abundance and a shifting prey base for harbor seals.

Q fever is a zoonotic disease caused by the bacterium Coxiella burnetii. Humans are commonly exposed via inhalation of aerosolized bacteria derived from the waste products of domesticated sheep and goats, and particularly from products generated during parturition. However, many other species can be infected with C. burnetii, and the host range and full zoonotic potential of C. burnetii is unknown. Two cases of C. burnetii infection in marine mammal placenta have been reported, but it is not known if this infection is common in marine mammals. To address this issue, placenta samples were collected from Pacific harbor seals (Phoca vitulina richardsi), harbor porpoises (Phocoena phocoena), and Steller sea lions (Eumetopias jubatus). Coxiella burnetii was detected by polymerase chain reaction (PCR) in the placentas of Pacific harbor seals (17/27), harbor porpoises (2/6), and Steller sea lions (1/2) collected in the Pacific Northwest. A serosurvey of 215 Pacific harbor seals sampled in inland and outer coastal areas of the Pacific Northwest showed that 34.0% (73/215) had antibodies against either Phase 1 or Phase 2 C. burnetii. These results suggest that C. burnetii infection is common among marine mammals in this region.

Phocid herpesvirus-1 (PhHV-1, subfamily Alphaherpesvirinae) was isolated from harbor seals (Phoca vitulina vitulina) in the Netherlands in 1985, and was subsequently identified in Pacific harbor seals (Phoca vitulina richardsi) from California, USA in the 1990s. PhHV-1-associated pathology was first recognized in harbor seal carcasses submitted to a veterinary diagnostic laboratory in Abbotsford, British Columbia, Canada in 2000, and 63 cases were identified by 2008. A review of these cases indicated that PhHV-1-associated disease is widespread in harbor seals in the wild and within rehabilitation facilities in the coastal northeastern Pacific (including British Columbia, Canada, and Washington, USA). Morbidity and mortality occurred primarily in neonatal and weanling seal pups, and was due to PhHV-1 alone, or in combination with other disease processes. All cases occurred between July and October, corresponding to the pupping and weaning seasons in this area. Although previous publications have described the prevalence of antibody to PhHV-1 in harbor seals from British Columbia, Canada and Washington, USA this is the first study to focus on the epidemiology and pathology of the virus in this region.