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We isolated a novel reassortant influenza A(H10N7) virus from a harbor seal in British Columbia, Canada, that died from bronchointerstitial pneumonia. The virus had unique genome constellations involving lineages from North America and Eurasia and polymerase basic 2 segment D701N mutation, associated with adaptation to mammals.

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.

As part of an ongoing investigation of harbor seal (Phoca vitulina) mortalities within Puget Sound, Washington State, United States, between October 2007 and July 2008, 25 seal cases were submitted for histopathology and ancillary diagnostic testing, including additional attempted virus isolation. In vitro granular and refractile cytopathic effects (CPE) were consistently observed in Vero.DogSLAMtag cells inoculated with tissue homogenates from three seals. Transmission electron microscopy of infected Vero.DogSLAMtag cells revealed cytoplasmic clusters of icosahedral viral particles morphologically consistent with members of the family Reoviridae. The complete genome of a novel species within the genus Orthoreovirus, tentatively named phocid orthoreovirus 1 (PhRV1), was determined by next-generation sequencing and confirmed by rt-PCR in isolates from the three harbor seals. This is the first report of an orthoreovirus infection associated with dead stranded harbor seals. Aside from the CPE and ultrastructural findings, no consistent signalment, gross pathology, histopathology, or ancillary diagnostic findings were identified with PhRV1 infection. Further research is needed to determine the prevalence, tissue tropism, transmission, pathogenicity, zoonotic potential, and host range of orthoreoviruses in pinnipeds. This study demonstrates the value of thorough necropsy investigations and a multidisciplinary team approach to advance our understanding of marine mammal health.

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.

The seal picornavirus 1, species Aquamavirus A, is currently the only recognized member of the genus Aquamavirus within the family Picornaviridae. The bear picornavirus 1 was recently proposed as the second species in the genus under the name aquamavirus B. Herein, we determined the complete genomes of two novel pinniped picornaviruses, the harbor seal picornavirus (HsPV) and the ribbon seal picornavirus (RsPV). The HsPV and the RsPV were isolated in Vero.DogSLAMtag cells from samples collected from stranded harbor (Phoca vitulina) and ribbon (Histriophoca fasciata) seals. RsPV-infected Vero.DogSLAMtag cells displaying extensive cytopathic effects were processed for transmission electron microscopy and revealed non-enveloped viral particles aggregated into paracrystalline arrays in the cytoplasm. A next-generation sequencing approach was used to recover the complete genomes of the HsPV and the RsPV (6,709 bp and 6,683 bp, respectively). Phylogenetic and genetic analyses supported the HsPV and the RsPV as members of the Aquamavirus genus. Based on these results, RsPV represents a novel strain of Aquamavirus A, while the HsPV is a novel strain of the proposed species aquamavirus B. These discoveries provide information on the evolutionary relationships and ultrastructure of aquamaviruses and expands the known host range of those viruses. Our results underscore the importance of the application of classical virology and pathology techniques coupled with high-throughput sequencing technologies for the discovery and characterization of pathogens in wild marine mammals.

Primary fungal diseases in marine mammals are rare. Mucormycosis, a disease caused by fungi of the order Mucorales, has been documented in few cetaceans and pinnipeds. In 2012, the first case of mucormycosis in the Pacific Northwest was documented in a dead stranded harbor porpoise (Phocoena phocoena) in Washington state. Since then, mucormycosis has been detected in a total of 21 marine mammals; fifteen harbor porpoises, five harbor seals (Phoca vitulina), and one southern resident killer whale (Orcinus orca). Infected animals were predominately found in the inland waters of Washington and British Columbia, and one harbor seal was recovered in northern Oregon. Fungal hyphae were detected histologically in a variety of tissues, including brain, lung, spleen, pancreas, kidneys, muscle, lymph nodes, and skin. Three fungal species were identified from seven cases by PCR screening or fungal culture; Rhizomucor pusillus (four cases), Lichtheimia corymbifera (two cases), and Cunninghamella bertholletiae. Underlying conditions such as emaciation, current or recent pregnancy, multisystemic parasitism, protozoal infection, and herpesvirus were found in several affected animals. Reasons for the appearance and subsequent increase of these fungal infections in marine mammals are unknown. The emergence of this disease as a source of marine mammal mortality in the Pacific Northwest is of particular concern for endangered southern resident killer whales that spend time in this region. Current population-level stressors such as insufficient prey, high levels of contaminants, and noise pollution, could predispose them to these fatal infections.

Effective 'valving' in the upper aerodigestive tract (UAT) is essential to temporarily separate the digestive and respiratory pathways. Marine mammals are largely dedicated to feeding underwater, and in many cases swallowing prey whole. In seals, little work has been done to explore the anatomy and function of the UAT in the context of valving mechanisms that function to separate food and air pathways. Here we use videofluoroscopy, gross dissection, histology and computed tomography (CT) renderings to explore the anatomy of the larynx and soft palate in the harbour seal (

The harbor seal (Phoca vitulina richardii) population in the Salish Sea has been at equilibrium since the mid-1990s. This stable population of marine mammals resides relatively close to shore near a large human population and offers a novel opportunity to evaluate whether disease acts in a density-dependent manner to limit population growth. We conducted a retrospective analysis of harbor seal stranding and necropsy findings in the San Juan Islands sub-population to assess age-related stranding trends and causes of mortality. Between January 01, 2002 and December 31, 2018, we detected 882 harbor seals that stranded and died in San Juan County and conducted necropsies on 244 of these animals to determine primary and contributing causes of death. Age-related seasonal patterns of stranded animals were evident, with pups found in the summer, weaned pups primarily recovered during fall, and adults and sub-adults recovered in summer and fall. Pups were the most vulnerable to mortality (64% of strandings). Pups predominantly died of nutritional causes (emaciation) (70%), whereas sub-adults and adults presented primarily with clinical signs and gross lesions of infectious disease (42%) and with non-anthropogenic trauma (27%). Primary causes of weaned pup mortality were distributed equally among nutritional, infectious, non-anthropogenic trauma, and anthropogenic trauma categories. Nutritional causes of mortality in pups were likely related to limitations in mid- and late-gestational maternal nutrition, post-partum mismothering, or maternal separation possibly related to human disturbance. Infectious causes were contributing factors in 33% of pups dying of nutritional causes (primarily emaciation–malnutrition syndrome), suggesting an interaction between poor nutritional condition and enhanced susceptibility to infectious diseases. Additional primary causes of harbor seal mortality were related to congenital disorders, predation, human interaction, and infections, including zoonotic and multidrug-resistant pathogens. Bottom-up nutritional limitations for pups, in part possibly related to human disturbance, as well as top-down predatory influences (likely under-represented through strandings) and infectious disease, are important regulators of population growth in this stable, recovered marine mammal population.

Approximately 5,000 Pacific harbor seals (

Cryptococcosis has been reported in marine mammals in the northeastern Pacific with increasing frequency in the last 15 yr. Although a variety of cetaceans have been diagnosed with cryptococcosis, Cryptococcus gattii has not been reported in pinnipeds. We document C. gattii VGIIa in a harbor seal ( Phoca vitulina ) pup and in an unrelated adult. Both animals were presented to Vancouver Aquarium's Marine Mammal Rescue Centre (VAMMRC) with generalized weakness, dehydration, respiratory compromise, minimally responsive mentation, and suboptimal body condition. Necropsy and histopathology findings were consistent in both animals and featured generalized lymphadenopathy, bronchopneumonia, and meningoencephalitis with intralesional yeast and fungemia. Cryptococcal serum antigen titers were ≥1,024 in both animals. Fungal culture of lung and lymph nodes confirmed C. gattii . Exposure was likely via inhalation prior to presentation to VAMMRC, and C. gattii infection was the proximate cause of death. This report expands the range of susceptible host species as C. gattii continues to emerge as a pathogen of concern in marine mammals in the northeastern Pacific.

In July 2013, a stranded harbor seal (Phoca vitulina) died giving birth to conjoined fetuses. The twins were joined at the abdomen and thoracolumbar spine with the vertebral axis at 180°. The cause of this unique anomaly--a first for this species--was not identified.

Approximately 5,000 Pacific harbor seals (Phoca vitulina richardii) reside year-round in San Juan County (SJC), Washington (US) in the center of the binational Salish Sea. We retrospectively analyzed total cadmium (Cd), copper (Cu), iron (Fe), mercury (Hg), magnesium (Mg), manganese (Mn), lead (Pb), selenium (Se), and zinc (Zn) in livers of dead stranded harbor seals (n=57) collected in SJC between 2009 and 2012 to identify age-related and regional patterns of trace element exposure. Consistent with prior studies of contaminants in pinnipeds, Hg, Cd, and Se concentrations increased with age, and Se:Hg molar ratios approached 1:1 in adult seals. Concentrations of Cd and Hg were below putative marine mammal toxicity thresholds. Mercury concentrations were comparable among Salish Sea populations. Although SJC is less urbanized with fewer industrial inputs than South Puget Sound (SPS), SJC nonpups had greater concentrations of Cd, Cu, and Zn, and pups had greater concentrations of Zn compared to SPS seals. We hypothesize these regional differences could be due to prey preference and availability or to natural geochemical processes. Reported concentrations inform future sampling protocols and can assist in tracking long-term temporal and spatial trends of trace elements in marine organisms.

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.

Harbor Seals (Phoca vitulina) are the most common and widely distributed pinniped in Washington State coastal waters. Serving as sentinels of marine ecosystem health, stranded animals are useful in detecting environmental disease and contaminant levels. From 2004 to 2010, we examined mortality rates and causes of death of Harbor Seal pups at Smith Island, a principal haulout site in the eastern Strait of Juan de Fuca, Washington, conducting 21 site surveys during the pupping season (June through August). We documented and externally examined 245 dead pups and of these, 72 were deemed suitable for more detailed internal examination and were collected for necropsy to determine cause of death. Minimum estimated neonatal mortality varied widely by year and ranged from 3 to 25%. The highest number of dead pups, nearly half of the total for the study, were found in 2005; this was also the year with the highest estimate of pups born and highest proportion of pups born that were documented dying. Infection was the leading primary cause of death in most years including 2005, when 40% of the pups died from an infectious process. The 2nd leading cause of death was malnutrition; other causes included prematurity and dystocia. This study documents some of the major annual differences that can occur in both mortality rates and causes of death in Harbor Seals.

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.

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.

Between 1998 and 2008, 15 cases of segmental to diffuse hemorrhagic to necrohemorrhagic enterocolitis were diagnosed in neonatal and weaned juvenile harbor seals (Phoca vitulina) presented from the Vancouver Aquarium Marine Mammal Rescue Centre for rehabilitation. Based on a combination of gross pathology, histopathology, bacterial isolation, and toxin testing, Clostridium difficile enterocolitis was diagnosed. Most pups were anorexic or inappetant and died acutely with few other premonitory signs. Due to ongoing clinical concerns and possible emergence of this pathogen at the facility, efforts to better characterize the disease and understand the epidemiology of C. difficile was initiated in 95 harbor seal pups presented for rehabilitation in a single stranding season. Fecal samples were collected on admission, following completion of antibiotic treatment, and also prerelease or postmortem. All samples were collected fresh and submitted either directly or stored frozen. Fecal samples were inoculated into selective media for culture and screened by enzyme-linked immunosorbant assay (ELISA) for C. difficile toxins A, B, or both. Results of the 95 seals in the study were as follows: on hospital admit 72 seals were sampled, 10 were culture positive, 12 were ELISA positive; following antibiotic therapy 46 seals were sampled noting three culture positive and nine ELISA positive; prior to release 58 seals were sampled noting zero culture positive and one ELISA positive; and on postmortem exam seven seals were sampled noting zero culture positive and two ELISA positive. Clostridium difficile was not deemed to be the cause of death in any of the animals. Although the exact mechanism of disease is unknown, this study suggests that C. difficile infection is not a significant cause of mortality and may be part of the normal flora in harbor seals undergoing rehabilitation. Morbidity and mortality from this bacterium can likely be minimized by judicious use of antibiotics, effective biosecurity-biocontainment protocols, and clean husbandry practices.

Department of Wildlife, Humboldt State University, Arcata, California 95521 USA; philpcapitolo@hotmail. com (PJC); Carter Biological Consulting, 1015 Hampshire Road, Victoria, British Columbia V8S 4S8 Canada (HRC); US Fish and Wildlife Service, San Francisco Bay National Wildlife Refuge Complex, PO Box 524, Newark, California 94560 USA (GJM, MWP); Present Address (MWP): US Fish and Wildlife Service, Red Rock Lakes National Wildlife Refuge, 27820 South Centennial Road, Lima, Montana 59739 USA. Submitted 9 March 2005, accepted 27 July 2005. Corresponding Editor: CJ Ralph.

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.

Polychlorinated biphenyls and other persistent organic pollutants have been associated with immunotoxicity and outbreaks of (infectious) disease in marine mammals by rendering them vulnerable to infection by pathogens such as viruses and bacteria. In an immunotoxicological study of free-ranging harbor seals (Phoca vitulina), we obtained samples of blood and blubber from seal pups that were live-captured from two remote and two near-urban sites in British Columbia, Canada, and Washington state, USA. Using these samples, we quantified hematology, innate immune function, adaptive immune function, and polychlorinated biphenyl accumulation. While controlling for confounding factors (age, sex, and condition), univariate correlations between phagocytosis (r 2 = 0.30, p = 0.002), respiratory burst (r 2 =0.45, p= 0.000), T-lymphocyte function (r 2 = 0.16, p = 0.028), lymphocyte signaling (r 2 = 0.17, p = 0.025), and lymphocyte counts (r 2 = 0.29, p = 0.002), and polychlorinated biphenyl concentrations suggested chemical-associated immunotoxicity. Principal component analysis of immunological endpoints provided additional evidence of immunotoxic effects in seals. However, principal component analysis also identified a noncontaminant-related factor by distinguishing between seals inhabiting urban versus remote sites, with results being consistent with increased pathogen exposure. Elevated fecal coliform concentrations in water, and observations of terrestrial spill-over pathogens in local seals, further support the notion of biological pollution at these sites. Although our study highlights the role that environmental contaminants might play in rendering marine mammal populations vulnerable to disease through immunotoxicity, it also suggests that biological pollution represents an emerging conservation concern.