Tacoma, WA, United States
Tacoma, WA, United States

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Huggins J.L.,Collective | Raverty S.A.,Animal Health Center | Norman S.A.,Central Puget Sound Marine Mammal Stranding Network | Norman S.A.,Marine Med Marine Research | And 10 more authors.
Diseases of Aquatic Organisms | Year: 2015

In 2006, a marked increase in harbor porpoise Phocoena phocoena strandings were reported in the Pacific Northwest of the USA, resulting in the declaration of an unusual mortality event (UME) for Washington and Oregon to facilitate investigation into potential causes. The UME was in place during all of 2006 and 2007, and a total of 114 porpoises stranded during this period. Responders examined 95 porpoises; of these, detailed necropsies were conducted on 75 animals. Here we review the findings related to this event and how these compared to the years immediately before and after the UME. Relatively equal numbers among sexes and age classes were represented, and mortalities were attributed to a variety of specific causes, most of which were categorized as trauma or infectious disease. Continued monitoring of strandings during 4 yr following the UME showed no decrease in occurrence. The lack of a single major cause of mortality or evidence of a significant change or event, combined with high levels of strandings over several post-UME years, demonstrated that this was not an actual mortality event but was likely the result of a combination of factors, including: (1) a growing population of harbor porpoises; (2) expansion of harbor porpoises into previously sparsely populated areas in Washington's inland waters; and (3) a more well established stranding network that resulted in better reporting and response. This finding would not have been possible without the integrated response and investigation undertaken by the stranding network. © Inter-Research 2015.


Akmajian A.M.,Marine Mammal Investigations | Lambourn D.M.,Marine Mammal Investigations | Lance M.M.,Marine Mammal Investigations | Raverty S.,Animal Health Center | Gaydos J.K.,University of California at Davis
Journal of Wildlife Diseases | Year: 2012

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. © Wildlife Disease Association 2012.


Himworth C.G.,University of Saskatchewan | Haulena M.,Vancouver Aquarium | Lambourn D.M.,Marine Mammal Investigations | Gaydos J.K.,University of California at Davis | And 5 more authors.
Journal of Wildlife Diseases | Year: 2010

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. © Wildlife Disease Association 2010.


Lambourn D.M.,Marine Mammal Investigations | Garner M.,Northwest ZooPath | Ewalt D.,National Veterinary Services Laboratories | Raverty S.,Animal Health Center | And 5 more authors.
Journal of Wildlife Diseases | Year: 2013

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. © Wildlife Disease Association 2013.


Alava J.J.,Simon Fraser University | Alava J.J.,Canadian Department of Fisheries and Oceans | Lambourn D.,Marine Mammal Investigations | Olesiuk P.,Canadian Department of Fisheries and Oceans | And 4 more authors.
Chemosphere | Year: 2012

Polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls (PCBs) were measured in blubber biopsy samples from 22 live-captured Steller sea lions (Eumetopias jubatus) that had just entered the Strait of Georgia, British Columbia, Canada, for their overwintering feeding season ∑PBDE ranged from 50μgkg -1 (lipid weight) in adult females to 3780μgkg -1 in subadult individuals ∑PCBs ranged from 272μgkg -1 in adult females to 14280μgkg -1 in subadult individuals. While most PBDE and PCB congeners were transferred through milk to pups, PCBs with logK OW>7.0 (PCBs 206, 207, 208 and 209) appeared constrained, resulting in a lighter mixture in pups compared to adult females. The ratio of individual PCB congeners by metabolic group (Groups I, II, III, IV and V) to PCB-153 regressed against length of males suggested poor biotransformation of these compounds (slopes did not differ from zero, p>0.05). PBDE congeners 49, 99, 153 and 183 appeared bioaccumulative (slopes of ratio BDE/PCB 153 versus length were higher than zero, p<0.05), but the dominance of the single congener, BDE-47 (64% of total PBDEs), likely due in part to debromination pathways, reduced our ability to explore congener-specific dynamics of PBDEs in these pinnipeds. With 80% of our Steller sea lions exceeding a recent toxicity reference value for PCBs, the fasting-associated mobilization of these contaminants raises concerns about a heightened vulnerability to adverse effects during annual migrations. © 2012 Elsevier Ltd.


London J.M.,National Oceanic and Atmospheric Administration | Hoef J.M.,National Oceanic and Atmospheric Administration | Jeffries S.J.,Marine Mammal Investigations | Lance M.M.,Marine Mammal Investigations | Boveng P.L.,National Oceanic and Atmospheric Administration
PLoS ONE | Year: 2012

The goal of this study was to model haul-out behavior of harbor seals (Phoca vitulina) in the Hood Canal region of Washington State with respect to changes in physiological, environmental, and temporal covariates. Previous research has provided a solid understanding of seal haul-out behavior. Here, we expand on that work using a generalized linear mixed model (GLMM) with temporal autocorrelation and a large dataset. Our dataset included behavioral haul-out records from archival and VHF radio tag deployments on 25 individual seals representing 61,430 seal hours. A novel application for increased computational efficiency allowed us to examine this large dataset with a GLMM that appropriately accounts for temporal autocorellation. We found significant relationships with the covariates hour of day, day of year, minutes from high tide and year. Additionally, there was a significant effect of the interaction term hour of day: day of year. This interaction term demonstrated that seals are more likely to haul out during nighttime hours in August and September, but then switch to predominantly daylight haul-out patterns in October and November. We attribute this change in behavior to an effect of human disturbance levels. This study also examined a unique ecological event to determine the role of increased killer whale (Orcinus orca) predation on haul-out behavior. In 2003 and 2005 these harbor seals were exposed to unprecedented levels of killer whale predation and results show an overall increase in haul-out probability after exposure to killer whales. The outcome of this study will be integral to understanding any changes in population abundance as a result of increased killer whale predation.


Huber H.R.,National Oceanic and Atmospheric Administration | Dickerson B.R.,National Oceanic and Atmospheric Administration | Jeffries S.J.,Marine Mammal Investigations | Lambourn D.M.,Marine Mammal Investigations
Canadian Journal of Zoology | Year: 2012

Washington harbor seals (Phoca vitulina richardii (Gray, 1864)) are currently managed as two stocks: Washington Coastal Stock and Washington Inland Waters Stock. Previous analysis of mitochondrial DNA (mtDNA) in Washington harbor seals showed four geographically and genetically distinct populations. In this study of biparentally inherited nuclear DNA, we analyzed nine microsatellite loci on 482 samples of unweaned pups from nine locations in Washington State and the US-Canadian transboundary waters to determine if there were differences in gene flow between males and females. We found the same four genetically and geographically distinct populations as the analysis of maternally inherited mtDNA: Washington Coast, north Inland Waters, Hood Canal, and south Puget Sound. We recommend that the coastal stock remain as is, but the harbor seals in the Washington Inland Waters should be managed as three distinct populations rather than one.


Huber H.R.,National Oceanic and Atmospheric Administration | Jeffries S.J.,Marine Mammal Investigations | Lambourn D.M.,Marine Mammal Investigations | Dickerson B.R.,National Oceanic and Atmospheric Administration
Canadian Journal of Zoology | Year: 2010

We examined the pupping phenology and genetic variation between the currently defined stocks of harbor seals, Phoca vitulina richardsi (Gray, 1864), in Washington's coastal and inland waters and looked in detail at genetic variation within the inland waters of Washington. We analyzed mtDNA variation in 552 harbor seals from nine areas in Washington State and the Canada-US transboundary waters. A total of 73 haplotypes were detected; 37 individuals had unique haplotypes. Pupping phenology and levels of genetic variation between the outer coastal stock (WA Coastal Estuaries, WA North Coast) and the inland waters stock (British Columbia, Boundary Bay, San Juan Islands, Smith/Minor Islands, Dungeness Spit, Hood Canal, Gertrude Island) corroborated the appropriateness of the present stock boundary. However, within the inland waters stock, Hood Canal and Gertrude Island were significantly different from the coastal stock, from the rest of the inland waters stock, and from each other. This indicates a total of four genetically distinct groups in Washington State, suggesting that managing the inland waters as a single stock may be erroneous.


PubMed | Marine Mammal Investigations
Type: Journal Article | Journal: Journal of wildlife diseases | Year: 2014

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.


PubMed | Marine Mammal Investigations
Type: Journal Article | Journal: Journal of wildlife diseases | Year: 2012

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.

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