Seasonal and developmental differences in blubber stores of beluga whales in Bristol Bay, Alaska using high-resolution ultrasound.

Diving mammals use blubber for a variety of structural and physiological functions, including buoyancy, streamlining, thermoregulation, and energy storage. Estimating blubber stores provides proxies for body condition, nutritional status, and health. Blubber stores may vary topographically within individuals, across seasons, and with age, sex, and reproductive status; therefore, a single full-depth blubber biopsy does not provide an accurate measure of blubber depth, and additional biopsies are limited because they result in open wounds. We examined high-resolution ultrasound as a noninvasive method for assessing blubber stores by sampling blubber depth at 11 locations on beluga whales in Alaska. Blubber mass was estimated as a proportion of body mass (40% from the literature) and compared to a function of volume calculated using ultrasound blubber depth measurements in a truncated cone. Blubber volume was converted to total and mass-specific blubber mass estimates based on the density of beluga blubber. There was no significant difference in mean total blubber mass between the 2 estimates (R2 = 0.88); however, body mass alone predicted only 68% of the variation in mass-specific blubber stores in juveniles, 7% for adults in the fall, and 33% for adults in the spring. Mass-specific blubber stores calculated from ultrasound measurements were highly variable. Adults had significantly greater blubber stores in the fall (0.48±0.02kg/kgMB) than in the spring (0.33±0.02kg/kgMB). There was no seasonal effect in juveniles. High-resolution ultrasound is a more powerful, noninvasive method for assessing blubber stores in wild belugas, allowing for precise measurements at multiple locations.

Seasonal hematology and serum chemistry of wild beluga whales (Delphinapterus leucas) in Bristol Bay, Alaska, USA.

We collected blood from 18 beluga whales (Delphinapterus leucas), live-captured in Bristol Bay, Alaska, USA, in May and September 2008, to establish baseline hematologic and serum chemistry values and to determine whether there were significant differences in hematologic values by sex, season, size/age, or time during the capture period. Whole blood was collected within an average of 19 min (range=11-30 min) after the net was set for capture, and for eight animals, blood collection was repeated in a later season after between 80-100 min; all blood was processed within 12 hr. Mean hematocrit, chloride, creatinine, total protein, albumin, and alkaline phosphatase were significantly lower in May than they were in September, whereas mean corpuscular hemoglobin concentration, monocytes, phosphorous, magnesium, blood urea nitrogen, alanine aminotransferase, aspartate aminotransferase, γ-glutamyltranspeptidase, and creatinine kinase were significantly higher. Mean total protein, white blood cell count, neutrophils, and lymphocytes were significantly higher early in the capture period than they were later. No significant differences in blood analyte values were noted between males and females. Using overall body length as a proxy for age, larger (older) belugas had lower white blood cell, lymphocyte, and eosinophil counts as well as lower sodium, potassium, and calcium levels but higher creatinine levels than smaller belugas. These data provide values for hematology and serum chemistry for comparisons with other wild belugas.

Escherichia albertii in wild and domestic birds.

Escherichia albertii has been associated with diarrhea in humans but not with disease or infection in animals. However, in December 2004, E. albertii was found, by biochemical and genetic methods, to be the probable cause of death for redpoll finches (Carduelis flammea) in Alaska. Subsequent investigation found this organism in dead and subclinically infected birds of other species from North America and Australia. Isolates from dead finches in Scotland, previously identified as Escherichia coli O86:K61, also were shown to be E. albertii. Similar to the isolates from humans, E. albertii isolates from birds possessed intimin (eae) and cytolethal distending toxin (cdtB) genes but lacked Shiga toxin (stx) genes. Genetic analysis of eae and cdtB sequences, multilocus sequence typing, and pulsed-field gel electrophoresis patterns showed that the E. albertii strains from birds are heterogeneous but similar to isolates that cause disease in humans.

Expression and self-assembly of virus-like particles from two genotypes of marine vesiviruses and development of an ELISA for the detection of antibodies.

Sequences encoding the major and minor capsid proteins (VP1 and VP2) from two marine vesivirus isolates (Steller sea lion viruses V810 and V1415) were engineered for expression of virus-like particles (VLPs) in the baculovirus system. The resulting VLPs were morphologically similar to native vesivirus virions. Purified VLPs were probed in immunoblots with pooled antisera specific for nine San Miguel sea lion virus (SMSV) types, and a predominant protein of approximately 60kDa was detected. An enzyme linked immunosorbent assay (ELISA) for the detection of antibodies was developed in which the VLPs served as antigen. The VLPs were adsorbed to the wells of a microplate, and the specificity of the ELISA was established with hyperimmune sera raised against 24 serotypes of the genus Vesivirus. The ELISA was used to screen for the presence of vesivirus specific antibodies in the sera of free-ranging Steller sea lions. The ELISA results demonstrated that Steller sea lions that inhabit the Pacific Ocean waters of southeast Alaska are widely exposed to antigenically related marine vesiviruses, while no previous exposure could be demonstrated using VLP antigens in 17 Steller sea lions from the Aleutian Islands. The broad reactivity of these VLPs and their non-infectious nature will facilitate global sero-epidemiological studies aimed at determining the incidence and prevalence of marine vesiviruses in mammals that inhabit the Pacific and Atlantic oceans as well as susceptible terrestrial animals.

Phocine distemper virus in northern sea otters in the Pacific Ocean, Alaska, USA.

Phocine distemper virus (PDV) has caused 2 epidemics in harbor seals in the Atlantic Ocean but had never been identified in any Pacific Ocean species. We found that northern sea otters in Alaska are infected with PDV, which has created a disease threat to several sympatric and decreasing Pacific marine mammals.

Genomic characterization of novel marine vesiviruses from Steller sea lions (Eumetopias jubatus) from Alaska.

Marine vesiviruses were isolated in cell culture from oral and rectal swabs and vesicular fluid from Alaskan Steller sea lions (SSL; Eumetopias jubatus). Further characterization by RT-PCR, complete genomic sequencing, and phylogenetic analyses indicated that these viruses are most closely related to the marine vesiviruses, but are distinct viruses and represent two novel genotypes. The complete genome of these two SSL isolates was sequenced after cloning their viral cDNA. The genomes were found to be 8302 and 8305 nucleotides in length, organized in three open reading frames and contained 5' and 3' untranslated regions (UTR) of 19 and 180 nucleotides, respectively. The complete genomes of both SSL viruses were most closely related to each other and shared 83.0% nucleotide identity. Using the very limited number of complete genomic vesivirus sequences available in the NCBI database, these novel SSL vesiviruses seem most closely related to vesicular exanthema of swine virus-A48 and least related to rabbit vesivirus and walrus calicivirus. Specific antiserum against some evolutionary closer marine vesiviruses did not neutralize these isolates supporting the novel nature of these SSL viruses.

Effects of climate change on Arctic marine mammal health.

The lack of integrated long-term data on health, diseases, and toxicant effects in Arctic marine mammals severely limits our ability to predict the effects of climate change on marine mammal health. The overall health of an individual animal is the result of complex interactions among immune status, body condition, pathogens and their pathogenicity, toxicant exposure, and the various environmental conditions that interact with these factors. Climate change could affect these interactions in several ways. There may be direct effects of loss of the sea ice habitat, elevations of water and air temperature, and increased occurrence of severe weather. Some of the indirect effects of climate change on animal health will likely include alterations in pathogen transmission due to a variety of factors, effects on body condition due to shifts in the prey base/food web, changes in toxicant exposures, and factors associated with increased human habitation in the Arctic (e.g., chemical and pathogen pollution in the runoff due to human and domestic-animal wastes and chemicals and increased ship traffic with the attendant increased risks of ship strike, oil spills, ballast pollution, and possibly acoustic injury). The extent to which climate change will impact marine mammal health will also vary among species, with some species more sensitive to these factors than others. Baseline data on marine mammal health parameters along with matched data on the population and climate change trends are needed to document these changes.

Infectious disease and the decline of Steller sea lions (Eumetopias jubatus) in Alaska, USA: insights from serologic data.

Serologic data were examined to determine whether infectious disease may have played a role in the decline of Steller sea lions (Eumetopias jubatus) in the Gulf of Alaska and Aleutian Islands, USA. Available published data, unpublished data, and recent collections (1997-2000) were compared and reviewed. Data were stratified by geography to compare the declining western Alaskan population in the Aleutian Islands through eastern Prince William Sound to the increasing population in southeastern Alaska. Prevalences of antibodies from the 1970s to the early 1990s were noted for Leptospira interrogans, Chlamydophila psittaci, Brucella spp., phocid herpesvirus-1, and calciviruses. Serum samples collected from 1997-2000 were tested for antibodies to these agents as well as to marine mammal morbilliviruses, canine parvovirus, and canine adenovirus-1 and -2. Conclusions could not be drawn about changes in antibody prevalence to these agents during the decline of Steller sea lions, however, because data were incomplete or not comparable as a result of inconsistencies in testing techniques. Despite these shortcomings, results provided no convincing evidence of significant exposure of Steller sea lions to morbilliviruses, Brucella spp., canine parvovirus, or L. interrogans. Steller sea lions have been exposed to phocid herpesviruses, caliciviruses, canine adenovirus, and C. psittaci or to cross-reactive organisms in regions of both increasing and decreasing sea lion abundance. Based on similar antibody prevalence estimates from the increasing and decreasing populations, these agents are unlikely to have been the primary cause of the population decline. They may have contributed to the decline or impeded population recovery, however, because of undetected mortality and morbidity or reductions of fecundity and body condition in animals under other stresses. Systematic monitoring for disease agents and their effects is needed to determine whether infectious disease currently plays a role in the decline and lack of recovery of Steller sea lions.

Poxvirus infection of Steller sea lions (Eumetopias jubatus) in Alaska.

Lesions suggestive of poxvirus infection were observed in two Steller sea lions (Eumetopias jubatus) in Alaska during live capture-and-release studies during 2000 and 2001. Both of these animals, female pups in poor body condition, were from Prince William Sound; this population is part of the declining western stock. Umbilicated, typically ulcerated dermal nodules were present, primarily on the fore flippers in one case, and over most of the body in the second case. Histologically, there were discrete masses in the superficial dermis composed of epithelial cells, some of which contained eosinophilic intracytoplasmic inclusion bodies. Negative staining of skin biopsy homogenates demonstrated the presence of orthopoxvirus-like particles. Total DNA extracted from skin biopsies were analyzed by polymerase chain reaction (PCR) using primers that targeted the DNA polymerase and DNA topoisomerase genes. These primers directed the amplification of fragments 543 base pairs (bp) and 344 bp, respectively, whose deduced amino acid sequences indicated the presence of a novel poxvirus within the Chordopoxvirinae subfamily. Comparison of these amino acid sequences with homologous sequences from members of the Chordopoxvirinae indicated highest identity with orthopoxviruses.