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From February to May 2021, four nonmigratory rams from the Radium-Stoddart bighorn sheep (BHS; Ovis canadensis) herd in the Rocky Mountains of southeastern British Columbia, Canada, died from infection with the giant liver fluke, Fascioloides magna. Affected animals were emaciated, weak, and lethargic or were found dead. Gross lesions, histopathology, and parasite burdens were consistent with those reported in experimentally infected BHS, domestic sheep, and other aberrant hosts. Although BHS range does not typically overlap with fluke-contaminated aquatic habitats, the change in migratory behavior recently observed in some Radium-Stoddart rams may have exposed the affected animals to F. magna. We describe clinical signs and gross and histopathologic findings of hepatobiliary trematodiasis associated with F. magna in free-ranging BHS. From experimental data and our findings, giant liver fluke is pathogenic and is a threat to the conservation of the Radium-Stoddart BHS herd and other BHS herds in endemic F. magna regions.

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.

Coxiella burnetii is an intracellular bacterial pathogen that can be associated with significant reproductive disease or acute mortality in livestock and wildlife. A novel marine mammal-associated strain of C. burnetii has been identified in pinnipeds of the northwestern Pacific Ocean. Little is known about C. burnetii infection in regard to reproductive success or population status. Our objective was to characterize the severity and extent of histologic lesions in 117 opportunistically collected placentas from presumed-normal northern fur seals (Callorhinus ursinus) in July 2011 on St. Paul Island, Alaska, US, where a high placental prevalence of C. burnetii had been reported. Sections were examined by histology and immunohistochemistry and impression smears with modified acid-fast stain. The nature and frequency of histologic changes were compared with target COM1 PCR-confirmed C. burnetii positive and negative placentas. Overall, histologic changes were similar to placental lesions described in aborting ruminants; however, changes were variable within and between placentas. Vasculitis and occasional intracellular bacteria were seen only in C. burnetii PCR-positive placentas. Dystrophic mineralization, edema, and inflammation were seen in PCR-positive and negative placentas, although they were statistically more common in PCR-positive placentas. Results suggest that C. burnetti and associated pathologic changes are multifocal and variable in placentas from these presumably live-born pups. Therefore, multiple sections of tissue from different placental areas should be examined microscopically, and screened by PCR, to ensure accurate diagnosis as the genomes per gram of placenta may not necessarily represent the severity of placental disease. These limitations should inform field biologists, diagnosticians, and pathologists how best to screen and sample for pathogens and histopathology in marine mammal placental samples.

Sarcocystis spp. are protozoan parasites that cause a spectrum of lesions in various hosts. Hepatic sarcocystosis and encephalitis have been described in captive American black bears (Ursus americanus) and polar bears (Ursus maritimus), and in a free-ranging grizzly bear (Ursus arctos horribilis), but have not previously been reported in free-ranging American black bears. This study aimed to characterize the presence and lesions associated with Sarcocystis spp. in free-ranging bears in British Columbia, Canada from samples submitted to the provincial diagnostic laboratory. From 2007 to 2019, 102 free-ranging American black bear and grizzly bear tissues were examined postmortem for sarcocystosis using histopathology and follow-up molecular diagnostics. Sarcocystosis was confirmed in 41 (40%) free-ranging bears including 39 American black bears and two grizzly bears. Microscopic lesions included multifocal necrotizing hepatitis, nonsuppurative encephalitis, and/or intramuscular sarcocysts with or without associated inflammation. Sarcocystosis was considered the cause of death in eight (20%) of these bears, exclusively in cubs of the year (

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.

Retrospective analysis of diagnostic findings from 30 marine-foraging river otter (Lontra canadensis) carcasses opportunistically acquired between 2003 and 2013 revealed trauma as the most common cause of mortality (47%). Within this focal population, causes of trauma included vehicular, gunshot, and one case of suspect intraspecific aggression. Other causes of death included idiopathic (20%), infectious (13%), metabolic (10%), nutritional (7%), and neoplasia (3%). One case of neoplasia, a pancreatic islet cell adenoma, was identified in a 12-yr-old female. In six animals, diffuse renal interstitial fibrosis and multifocal glomerulosclerosis of unknown clinical significance were noted.

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.

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.

Streptococcus phocae is a pathogen of marine mammals, although its pathogenicity remains poorly understood. Recovery of this bacterium from asymptomatic carriers suggests that it is an opportunistic pathogen. We investigated the role of S. phocae in naturally occurring disease and its significance as a pathogen based on postmortem investigations. Between 2007 and 2012, 1,696 whole carcasses, tissue samples, or both were submitted from the northeastern Pacific and Arctic Canada for diagnostic testing. Streptococcus phocae was cultured from phocids ( n=66), otariids ( n=12), harbor porpoises ( Phocoena phocoena; n=5), and sea otters ( Enhydra lutris; n=2). Pathologic manifestations of S. phocae-associated disease included localized, as well as systemic, inflammatory lesions with common findings of suppurative bronchopneumonia ( n=17) and bacteremia ( n=27). Lung lesions were frequently culture-positive for S. phocae, suggesting commensal colonization of the oropharynx with subsequent opportunistic infection of the respiratory tract during tissue injury, coinfection, immunosuppression, or other debilitating conditions. The presence of a positive spleen culture, and interpretations at necropsy and histopathology, were used to determine the presence of S. phocae bacteremia. Less frequent lesions that were culture positive for S. phocae included abscesses ( n=9), meningitis ( n=7), and cellulitis ( n=1). The majority of cases with S. phocae lesions featured pre-existing conditions that presumably contributed to some degree of debilitation or immunosuppression, including emaciation ( n=29), liver mercury accumulation ( n=29), trauma ( n=22), severe pulmonary or cardiovascular nematodiasis ( n=9), concurrent bacterial or viral infections ( n=8), or sarcocystosis ( n=6). These findings suggest that S. phocae could be characterized as an opportunistic pathogen, associated with debilitating conditions in stranded and rehabilitating marine mammals. Wildlife investigators can use these results to draw more definitive conclusions regarding positive S. phocae cultures during postmortem studies in marine mammals.

Previously, we reported the isolation of Bartonella henselae from the blood of harbor porpoises (Phocoena phocoena) and loggerhead sea turtles (Caretta caretta) from the North Carolina coast. Hematologic, pathologic, and microbiologic findings surrounding the death of a juvenile captive beluga in Vancouver initiated an outbreak investigation designed to define the molecular prevalence of Bartonella infection in belugas. Using polymerase chain reaction analyses targeting the intergenic spacer region (ITS), two B. henselae ITS strains were identified in 78% of captive and free-ranging hunter-harvested belugas. These findings may have public health implications and may influence aquarium management procedures for captive marine mammals.

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.

Salmonella enterica serovar New-port (Salmonella Newport) was isolated from multiple tissues in a neonate killer whale (Orcinus orca) that stranded dead in 2005 along the central coast of California, USA. Necrotizing omphaloarteritis and omphalo-phlebitis was observed on histologic examination suggesting umbilical infection was the route of entry. Genetic analysis of skin samples indicated that the neonate had an offshore haplotype. Salmonellosis has rarely been identified in free-ranging marine mammals and the significance of Salmonella Newport infection to the health of free-ranging killer whales is currently unknown.