Phocine Distemper Research Articles

Did algal toxin and Klebsiella infections cause the unexplained 2007 mass mortality event in Danish and Swedish marine mammals?

An unusual mass mortality event (MME) of harbour seals (Phoca vitulina) and harbour porpoises (Phocoena phocoena) occurred in Denmark and Sweden in June 2007. Prior to this incident, the region had experienced two MMEs in harbour seals caused by Phocine Distemper Virus (PDV) in 1988 and 2002. Although epidemiology and symptoms of the 2007 MME resembled PDV, none of the animals examined for PDV tested positive. Thus, it has been speculated that another – yet unknown – pathogen caused the June 2007 MME. To shed new light on the likely cause of death, we combine previously unpublished veterinary examinations of harbour seals with novel analyses of algal toxins and algal monitoring data. All harbour seals subject to pathological examination showed pneumonia, but were negative for PDV, influenza and coronavirus. Histological analyses revealed septicaemia in multiple animals, and six animals tested positive for Klebsiella pneumonia. Furthermore, we detected the algal Dinophysis toxin DTX-1b (1–115 ng g−1) in five seals subject to toxicology, representing the first time DTX-1b has been detected in marine vertebrates. However, no animals tested positive for both Klebsiella and toxins. Thus, while our relatively small sample size prevent firm conclusions on causative agents, we speculate that the unexplained MME may have been caused by a chance incidence of multiple pathogens acting in parallel in June 2007, including Dinophysis toxin and Klebsiella. Our study illustrates the complexity of wildlife MMEs and highlights the need for thorough sampling during and after MMEs, as well as additional research on and monitoring of DTX-1b and other algal toxins in the region.

California sea lion (Zalophus californianus) lymph-node explant reveals involvement and possible transcriptional regulation of SLAM and nectin-4 during phocine distemper virus infection.

Phocine distemper virus (PDV) is a significant cause of mortality for phocid seals; however, the susceptibility of otariids to this virus is poorly understood. The authors used a lymph-node explant culture system from California sea lions (Zalophus californianus, CSL) to investigate: (1) the role of signaling lymphocyte activation molecule (SLAM) and nectin-4 in PDV infection and their cellular expression patterns, (2) if PDV induces transcriptional regulation of cell-entry receptors, and (3) the involvement of apoptosis in PDV infection. PDV replicated in the lymph-node explants with peak replication 3 days post-infection (dpi), but the replication was not sustained 4 to 5 dpi. The PDV+ cells co-localized SLAM and nectin-4. These cells expressed IBA1, indicating a histiocytic lineage. Comparison of receptor expression between infected and mock-infected lymph nodes suggested transcriptional downregulation of both receptors during the initial stage of infection and upregulation during the late stage of infection, but the values lack of statistical significance. Cleaved caspase-3+ cells were slightly increased in the infected lymph nodes compared with the mock-infected lymph node from 1 to 4 dpi, but without statistical significance, and a few apoptotic cells co-expressed PDV. The results suggest that lymph-node explants might be an important model to study PDV pathogenesis. CSLs have the potential to be infected with PDV, as they express both cell-entry receptors in histiocytes. The lack of statistical significance in the PDV replication, transcriptional regulation of viral receptors, and changes in apoptosis suggest that although CSL might be infected by PDV, they might be less susceptible than phocid species.

SEROLOGIC RESPONSE AND ADVERSE EFFECTS OF RECOMBINANT CANINE DISTEMPER VACCINATION IN THREE AQUARIUM-HOUSED WALRUSES (ODOBENUS ROSMARUS).

Fatalities have been associated with phocine and canine distemper viruses in marine mammals, including pinnipeds. No data are available regarding distemper disease or vaccination in walruses. This study evaluates seroconversion and clinical adverse effects following administration of a canarypox-vectored recombinant distemper vaccination (two 1-ml doses, 3 wk apart) in three adult aquarium-housed walruses. Serum antibodies to distemper were measured using seroneutralization on blood samples collected under operant conditioning prior to and for 12 mon after vaccination or until titers were <32. All walruses seroconverted. Medium positive titers (64-128) were detected for 4 to 9.5 mon in two of three individuals. Interindividual variability was noted, with one individual displaying only low positive titers. Major swelling at the site of injection and lameness for a week following injection occurred in all three walruses. Further studies on dosing amount and interval are needed to make vaccine recommendations in this species.

Screening for Influenza and Morbillivirus in Seals and Porpoises in the Baltic and North Sea.

Historically, the seals and harbour porpoises of the Baltic Sea and North Sea have been subjected to hunting, chemical pollutants and repeated mass mortalities, leading to significant population fluctuations. Despite the conservation implications and the zoonotic potential associated with viral disease outbreaks in wildlife, limited information is available on the circulation of viral pathogens in Baltic Sea seals and harbour porpoises. Here, we investigated the presence of the influenza A virus (IAV), the phocine distemper virus (PDV) and the cetacean morbillivirus (CeMV) in tracheal swabs and lung tissue samples from 99 harbour seals, 126 grey seals, 73 ringed seals and 78 harbour porpoises collected in the Baltic Sea and North Sea between 2002-2019. Despite screening 376 marine mammals collected over nearly two decades, we only detected one case of PDV and two cases of IAV linked to the documented viral outbreaks in seals in 2002 and 2014, respectively. Although we find no evidence of PDV and IAV during intermediate years, reports of isolated cases of PDV in North Sea harbour seals and IAV (H5N8) in Baltic and North Sea grey seals suggest introductions of those pathogens within the sampling period. Thus, to aid future monitoring efforts we highlight the need for a standardized and continuous sample collection of swabs, tissue and blood samples across Baltic Sea countries.

Development and Validation of a Pan-Genotypic Real-Time Quantitative Reverse Transcription-PCR Assay To Detect Canine Distemper Virus and Phocine Distemper Virus in Domestic Animals and Wildlife.

Canine distemper virus (CDV) is an animal morbillivirus belonging to the family Paramyxoviridae and has caused major epizootics with high mortality levels in susceptible wildlife species. In recent years, the documented genetic diversity of CDV has expanded, with new genotypes identified in India, the Caspian Sea, and North America. However, no quantitative real-time PCR (RT-qPCR) that has been validated for the detection of all genotypes of CDV is currently available. We have therefore established and characterized a pan-genotypic probe-based RT-qPCR assay based on the detection of a conserved region of the phosphoprotein (P) gene of CDV. This assay has been validated using virus strains representative of six genotypes of CDV in different sample types, including frozen tissue, formalin-fixed paraffin-embedded tissue sections, and virus isolates. The primers and probe target sequences were sufficiently conserved to also enable detection of the phocine distemper virus strains responsible for epizootics in harbor seals in the North Sea in 1988 and 2002. Comparison with two recently published RT-qPCR assays for CDV showed that under equivalent conditions the primers and probe set reported in this study were more sensitive in detecting nucleic acids from an Asia-4 genotype, which displays sequence variation in primer and probe binding sites. In summary, this validated new pan-genotypic RT-qPCR assay will facilitate screening of suspected distemper cases caused by novel genotypes for which full genome sequences are unavailable and have utility in detecting multiple CDV strains in geographical regions where multiple genotypes cocirculate in wildlife.

Longitudinal analysis of pinnipeds in the northwest Atlantic provides insights on endemic circulation of phocine distemper virus.

Phocine distemper virus (PDV) is a morbillivirus that circulates within pinnipeds in the North Atlantic. PDV has caused two known unusual mortality events (UMEs) in western Europe (1988, 2002), and two UMEs in the northwest Atlantic (2006, 2018). Infrequent cross-species transmission and waning immunity are believed to contribute to periodic outbreaks with high mortality in western Europe. The viral ecology of PDV in the northwest Atlantic is less well defined and outbreaks have exhibited lower mortality than those in western Europe. This study sought to understand the molecular and ecological processes underlying PDV infection in eastern North America. We provide phylogenetic evidence that PDV was introduced into northwest Atlantic pinnipeds by a single lineage and is now endemic in local populations. Serological and viral screening of pinniped surveillance samples from 2006 onward suggest there is continued circulation of PDV outside of UMEs among multiple species with and without clinical signs. We report six full genome sequences and nine partial sequences derived from harbour and grey seals in the northwest Atlantic from 2011 through 2018, including a possible regional variant. Work presented here provides a framework towards greater understanding of how recovering populations and shifting species may impact disease transmission.

Emergence and radiation of distemper viruses in terrestrial and marine mammals.

Canine distemper virus (CDV) and phocine distemper virus (PDV) are major pathogens to terrestrial and marine mammals. Yet little is known about the timing and geographical origin of distemper viruses and to what extent it was influenced by environmental change and human activities. To address this, we (i) performed the first comprehensive time-calibrated phylogenetic analysis of the two distemper viruses, (ii) mapped distemper antibody and virus detection data from marine mammals collected between 1972 and 2018, and (iii) compiled historical reports on distemper dating back to the eighteenth century. We find that CDV and PDV diverged in the early seventeenth century. Modern CDV strains last shared a common ancestor in the nineteenth century with a marked radiation during the 1930s-1950s. Modern PDV strains are of more recent origin, diverging in the 1970s-1980s. Based on the compiled information on distemper distribution, the diverse host range of CDV and basal phylogenetic placement of terrestrial morbilliviruses, we hypothesize a terrestrial CDV-like ancestor giving rise to PDV in the North Atlantic. Moreover, given the estimated timing of distemper origin and radiation, we hypothesize a prominent role of environmental change such as the Little Ice Age, and human activities like globalization and war in distemper virus evolution.

Novel Morbillivirus as Putative Cause of Fetal Death and Encephalitis among Swine.

Morbilliviruses are highly contagious pathogens. The Morbillivirus genus includes measles virus, canine distemper virus (CDV), phocine distemper virus (PDV), peste des petits ruminants virus, rinderpest virus, and feline morbillivirus. We detected a novel porcine morbillivirus (PoMV) as a putative cause of fetal death, encephalitis, and placentitis among swine by using histopathology, metagenomic sequencing, and in situ hybridization. Phylogenetic analyses showed PoMV is most closely related to CDV (62.9% nt identities) and PDV (62.8% nt identities). We observed intranuclear inclusions in neurons and glial cells of swine fetuses with encephalitis. Cellular tropism is similar to other morbilliviruses, and PoMV viral RNA was detected in neurons, respiratory epithelium, and lymphocytes. This study provides fundamental knowledge concerning the pathology, genome composition, transmission, and cellular tropism of a novel pathogen within the genus Morbillivirus and opens the door to a new, applicable disease model to drive research forward.

Causes of Mortality of Northern Sea Otters (Enhydra lutris kenyoni) in Alaska From 2002 to 2012

Most of the world’s sea otters reside in Alaska, but there has never been an assessment of long-term mortality patterns for this keystone predator. We examined data collected from 780 northern sea otter (Enhydra lutris kenyoni)carcasses recovered in Alaska from 2002 to 2012 to evaluate the causes of mortality and risk factors associated with death. A smaller group (n= 144, 18%) of fresh non-frozen carcasses were included in a more detailed mortality analysis. Forty-four% of the fresh dead otters were determined to have died from infectious endocarditis, meningoencephalitis, and/or septicemia due to systemic streptococcosis (“Strepsyndrome”).Streptococcus lutetiensis, a member of theStreptococcus bovis/equinus(SB/E) group was most commonly isolated, although other members of the SB/E group were identified. There were fewer cases whereS. phocaeand other streptococci were isolated. A regression analysis revealed age and location risk factors forStrepsyndrome. Subadults were the highest risk age group, and otters recovered from the Kachemak Bay region were 3.6 times (95% CI: 2.2–5.9) more likely to die fromStrepsyndrome than otters recovered elsewhere. Diagnosis of thisStrepsyndrome had not been reported in other marine mammals in Alaska. Sporadic cases of septicemia and infectious endocarditis due toS. lutetiensishave been seen in the southern sea otter population in California. Other causes of death for the fresh otters included neurologic diseases (10%), trauma (8%), nutritional diseases (7%), cardiovascular diseases (7%), gastrointestinal diseases /parasites (6%), undetermined (5%), septicemia (3%), and neoplasia (3%). All other causes of death (oiling, hepatobiliary, fungal, marine biotoxins, pulmonary) were at or below 1%. Twenty percent of fresh animals were positive for phocine distemper virus (PDV) by polymerase chain reaction (PCR, 11/55), 18% seropositive for PDV (7/38), and paramyxovirus-like particles were demonstrated by electron microscopy within inclusion bodies from one animal. Low concentrations of the harmful algal bloom toxins domoic acid and saxitoxin were also detected in 26% and 22% of fresh animals, respectively. Protozoal disease was rare. These patterns of disease differ from sea otters in other regions and possible reasons are discussed.

Phocine distemper virus uses phocine and other animal SLAMs as a receptor but not human SLAM.

Morbilliviruses use the signaling lymphocyte activation molecule (SLAM) as a receptor to infect their hosts. Seals are almost the only animal species that show apparent infection with phocine distemper virus (PDV). Seal SLAM functioned as a PDV receptor. However, dolphin- and dog-SLAM molecules, but not human SLAM, were also fully functional PDV receptors. These data suggest that the host range of PDV is not simply determined by its SLAM usage. However, human nonsusceptibility to PDV infection may be at least partly attributable to the inability of PDV to use human SLAM as a receptor.

CANINE DISTEMPER VIRUS IN THE SEA OTTER (ENHYDRA LUTRIS) POPULATION IN WASHINGTON STATE, USA.

Before 2001, all serosurveys for morbilliviruses in sea otters (Enhydra lutris) in California, Washington, and Alaska, US, documented a 0% seroprevalence. The first published serologic detections of morbillivirus in sea otters occurred in 2001-02 in live-captured Washington sea otters, with a documented 80% seroprevalence. We conducted a retrospective study of sea otter cases from 1989 to 2010 compiled at the US Geological Survey, National Wildlife Health Center to identify cases of morbilliviral disease in Washington sea otters and to characterize the disease using immunohistochemistry, reverse transcription (RT)-PCR, genetic sequencing, virus isolation, and serology. We identified six cases of morbilliviral disease and 12 cases of morbilliviral infection in this population of sea otters during 2000-10. Significant histologic findings included inflammation in the white and gray matter of the brain characterized by lymphoplasmacytic perivascular cuffing, neuronal necrosis, and satellitosis in gray matter and by spongiosis, myelin degeneration, spheroids, and gemistocytes in white matter. Intranuclear and intracytoplasmic viral inclusion bodies were found in neurons, Purkinje cells, and glia. Immunohistochemistry for canine distemper virus (CDV) showed positive staining in neurons, glial cells, and cell processes. A pan-morbillivirus RT-PCR with subsequent restriction endonuclease digestion or sequencing identified CDV. Virus isolation was not successful. Two sea otters with morbilliviral encephalitis showed greater antibody titers to CDV than phocine distemper virus. Histologic changes were confined to the central nervous system and resembled neurologic canine distemper in domestic dogs. Cases of sea otters with morbilliviral infection without histologic changes could represent early infections or incompletely cleared sublethal infections. We found that morbillivirus was present in the Washington sea otter population as early as 2000, and we provide a description of the pathology of canine distemper in sea otters.

Pathological findings and survey for pathogens associated with reproductive failure in perinatal Steller sea lions Eumetopias jubatus.

Steller sea lions (SSLs) Eumetopias jubatus experienced a population decline in the 1960s, leading to the listing of the western stock as endangered and the eastern stock as threatened under the US Endangered Species Act. A decrease of births in the western stock beginning in the late 1960s indicates that reproductive failure may have contributed to the decline. We evaluated the role pathogens play in spontaneous abortions, premature births and neonatal deaths in SSLs. Archived tissues from carcasses (n = 19) collected in Alaska from 2002 to 2015 were tested by PCR for Coxiella burnetii, Brucella spp., Chlamydia and morbilliviruses. Animals examined included 47% premature pups, 32% aborted fetuses, 11% neonates and 11% intrauterine fetuses. Gross necropsy and histology findings were summarized in the context of the PCR findings. Tissues were negative for Chlamydia and C. burnetii. Brucella spp. were detected in the lung tissues of 3 animals, including 1 positive for the ST27 strain, the first detection of Brucella spp. DNA in SSLs. Phocine distemper virus was detected in 3 animals in 2 skin lesions and 1 placenta by hemi-nested diagnostic qRT-PCR. Both skin and the placental lesions had vesiculoulcerative changes, and 1 skin lesion contained inclusion bodies in syncytia and upon histologic examination, suggesting that the lesions may be associated with an infection reminiscent of phocine distemper virus, the first in SSLs. We highlight the continuing need for disease surveillance programs to improve our understanding of the prevalence and potential population impacts of these infectious disease agents for pinnipeds in Alaskan waters.

Viral emergence in marine mammals in the North Pacific may be linked to Arctic sea ice reduction

Climate change-driven alterations in Arctic environments can influence habitat availability, species distributions and interactions, and the breeding, foraging, and health of marine mammals. Phocine distemper virus (PDV), which has caused extensive mortality in Atlantic seals, was confirmed in sea otters in the North Pacific Ocean in 2004, raising the question of whether reductions in sea ice could increase contact between Arctic and sub-Arctic marine mammals and lead to viral transmission across the Arctic Ocean. Using data on PDV exposure and infection and animal movement in sympatric seal, sea lion, and sea otter species sampled in the North Pacific Ocean from 2001–2016, we investigated the timing of PDV introduction, risk factors associated with PDV emergence, and patterns of transmission following introduction. We identified widespread exposure to and infection with PDV across the North Pacific Ocean beginning in 2003 with a second peak of PDV exposure and infection in 2009; viral transmission across sympatric marine mammal species; and association of PDV exposure and infection with reductions in Arctic sea ice extent. Peaks of PDV exposure and infection following 2003 may reflect additional viral introductions among the diverse marine mammals in the North Pacific Ocean linked to change in Arctic sea ice extent.

Canine and Phocine Distemper Viruses: Global Spread and Genetic Basis of Jumping Species Barriers.

Canine distemper virus (CDV) and phocine distemper (PDV) are closely-related members of the Paramyxoviridae family, genus morbillivirus, in the order Mononegavirales. CDV has a broad host range among carnivores. PDV is thought to be derived from CDV through contact between terrestrial carnivores and seals. PDV has caused extensive mortality in Atlantic seals and other marine mammals, and more recently has spread to the North Pacific Ocean. CDV also infects marine carnivores, and there is evidence of morbillivirus infection of seals and other species in Antarctica. Recently, CDV has spread to felines and other wildlife species in the Serengeti and South Africa. Some CDV vaccines may also have caused wildlife disease. Changes in the virus haemagglutinin (H) protein, particularly the signaling lymphocyte activation molecule (SLAM) receptor binding site, correlate with adaptation to non-canine hosts. Differences in the phosphoprotein (P) gene sequences between disease and non-disease causing CDV strains may relate to pathogenicity in domestic dogs and wildlife. Of most concern are reports of CDV infection and disease in non-human primates raising the possibility of zoonosis. In this article we review the global occurrence of CDV and PDV, and present both historical and genetic information relating to these viruses crossing species barriers.

The status of harbour seals (Phoca vitulina) in the UK

Abstract Estimates of population size and trends are essential for effective conservation and management of wildlife populations. For harbour seals (Phoca vitulina), these data are required to fulfil statutory reporting obligations under national and international regulations. Aerial survey counts of harbour seals hauled out during their annual moult were used to estimate population sizes and trends at UK, regional (seal management unit, SMU) and local (Special Area of Conservation, SAC) scales. Results indicate that the current UK harbour seal population is similar to estimates from the late 1990s, but there were significant declines in some subpopulations and increases in others. Fitted trends suggest that the UK harbour seal population can be divided into three geographically coherent groups: South‐east populations (South‐East and North‐East England SMUs) have shown continuous increases punctuated by phocine distemper virus epidemics in 1988 and 2002; north‐east populations (East Scotland, Moray Firth, North Coast and Orkney, and Shetland SMUs) have declined since the late 1990s; north‐west populations (West Scotland, Western Isles, and South‐West Scotland SMUs) have remained stable or increased. Similar geographical population substructure is evident in recent population genetics results. Trends within SACs generally match SMU trends since 2002. Of the nine SACs designated for harbour seals, four declined (in East Scotland, Moray Firth, and North Coast and Orkney SMUs), four remained stable (in Shetland and West Scotland SMUs), and one increased (in South‐East England SMU). Large changes in relative abundance have resulted from differences in regional trends. For example, in 1996–1997 the West Scotland and North Coast and Orkney SMUs each held ~27% of the Great Britain population but now hold ~50% and ~4% respectively; in 1980, the South‐East England SMU population was ~50% that of the Wadden Sea population, but by 2016 it was equivalent to &lt;20% of the Wadden Sea count.

Marine Morbilliviruses: Diversity and Interaction with Signaling Lymphocyte Activation Molecules.

Epidemiological reports of phocine distemper virus (PDV) and cetacean morbillivirus (CeMV) have accumulated since their discovery nearly 30 years ago. In this review, we focus on the interaction between these marine morbilliviruses and their major cellular receptor, the signaling lymphocyte activation molecule (SLAM). The three-dimensional crystal structure and homology models of SLAMs have demonstrated that 35 residues are important for binding to the morbillivirus hemagglutinin (H) protein and contribute to viral tropism. These 35 residues are essentially conserved among pinnipeds and highly conserved among the Caniformia, suggesting that PDV can infect these animals, but are less conserved among cetaceans. Because CeMV can infect various cetacean species, including toothed and baleen whales, the CeMV-H protein is postulated to have broader specificity to accommodate more divergent SLAM interfaces and may enable the virus to infect seals. In silico analysis of viral H protein and SLAM indicates that each residue of the H protein interacts with multiple residues of SLAM and vice versa. The integration of epidemiological, virological, structural, and computational studies should provide deeper insight into host specificity and switching of marine morbilliviruses.

Phylogenomic insights to the origin and spread of phocine distemper virus in European harbour seals in 1988 and 2002.

The 1988 and 2002 phocine distemper virus (PDV) outbreaks in European harbour seals Phoca vitulina are among the largest mass mortality events recorded in marine mammals. Despite its large impact on harbour seal population numbers, and 3 decades of studies, many questions regarding the spread and temporal origin of PDV remain unanswered. Here, we sequenced and analysed 7123 bp of the PDV genome, including the coding and non-coding regions of the entire P, M, F and H genes in tissues from 44 harbour seals to shed new light on the origin and spread of PDV in 1988 and 2002. The phylogenetic analyses trace the origin of the PDV strain causing the 1988 outbreak to between May 1987 and April 1988, while the origin of the strain causing the 2002 outbreak can be traced back to between June 2001 and May 2002. The analyses further point to several independent introductions of PDV in 1988, possibly linked to a southward mass immigration of harp seals in the winter and spring of 1987-1988. The vector for the 2002 outbreak is unknown, but the epidemiological analyses suggest the subsequent spread of PDV from the epicentre in the Kattegat, Denmark, to haul-out sites in the North Sea through several independent introductions.

Dental anomalies and lesions in Eastern Atlantic harbor seals, Phoca vitulina vitulina (Carnivora, Phocidae), from the German North Sea.

Skulls of 1,901 Eastern Atlantic harbor seals (Phoca vitulina vitulina) were systematically studied for externally visible dental anomalies and lesions. The sample comprised 927 males and 974 female individuals, with age at death ranging between 1 week and 25 years. Most of the skulls originated from animals collected in 1988, when the population suffered from a mass mortality event caused by the phocine distemper virus (PDV). Mean age (± SD) of females (6.7 ± 6.4 years) was higher (p = 0.002) than that of males (5.9 ± 5.2 years). In 264 individuals, one or more teeth were missing either congenitally (n = 26 animals, 1.4%) or due to intravital loss (n = 238 animals, 12.5%). One male exhibited congenital absence of all teeth (anodontia). As this animal had been reported to be almost hairless, the condition was tentatively diagnosed as a case of hypohidrotic ectodermal dysplasia. Males were more frequently (p = 0.002) affected by intravital tooth loss (15.0%) than females (10.2%). Supernumerary teeth were found in 3.4% of the skulls, with females (4.7%) showing hyperodontia more frequently (p < 0.001) than males (1.9%). Fifty-nine individuals (3.1%; 28 males, 31 females, p = 0.84) exhibited abnormal tooth morphology. Tooth fractures were noted in 40 seals (2.1%), with males being more frequently affected than females (p = 0.017). Periapical lesions were diagnosed in 143 skulls, with a tendency (p = 0.05) for males (8.7%) to be more frequently affected than females (6.4%). Enamel hypoplasia was not observed in the study sample. Analyzing the occurrence of dental anomalies and lesions in wild mammals can substantially contribute to an assessment of population health and thereby broaden the basis for effective species conservation and informed management decisions.

Population Wide Decline in Somatic Growth in Harbor Seals—Early Signs of Density Dependence

The harbour seal populations of Danish and Swedish waters have had turbulent population dynamics during the last century. They were severely depleted by hunting in the beginning of the 20th century, followed by rapid recovery due to protective measures. They were victims to two mass mortalities caused by Phocine Distemper Virus (PDV) epidemics. Long term monitoring and intensive sampling during the last decades now allow analysis of population level phenomena in response to shifting population size. We compare somatic growth curves from several seal populations including 2 041 specimens with known age, length and population size at birth. Asymptotic body lengths of female harbour seals were 148 cm in all four regions in 1988, when seal abundances had been kept low by hunting for decades. Males were 158 cm, being 10 cm longer. However, in 2002 the asymptotic lengths of seals differed among regions. While seals in the Kattegat showed similar asymptotic lengths as in 1988, seals in the Skagerrak were significantly shorter, where both male and female asymptotic lengths declined by 7 cm. We estimate the area of available feeding grounds in the two sea regions and find the density of seals per square kilometre feeding ground to be three times greater in the Skagerrak compared to the Kattegat. Thus, the shorter body length of seals in the Skagerrak can be an early signal of density dependence. Hampered body growth is known to trigger a suite of changes in life history traits, including delayed age at sexual maturity, higher juvenile mortality and lowered fecundity. These mechanisms all point at a possible ‘’smooth route towards carrying capacity’’ with gradually reduced population growth rate as the main response to high population density. Recent aerial surveys confirm declining rates of population increase in the Skagerrak.

Osteoarthritis of the temporomandibular joint in the Eastern Atlantic harbour seal (Phoca vitulina vitulina) from the German North Sea: a study of the lesions seen in dry bone

BackgroundPathological changes and resulting functional impairment of the temporomandibular joint (TMJ) can substantially affect physical condition, morbidity, and mortality of wildlife species. Analysis of TMJ disorders is therefore of interest for the characterization of the health status of populations of wild mammals. This paper, for the first time, analyses the prevalence of TMJ osteoarthritis (TMJ-OA) and the spectrum of osteoarthritic bone lesions of the TMJ in the Eastern Atlantic harbour seal (Phoca vitulina vitulina), applying a standardized scoring system. Dry skulls of 1872 individuals from the German North Sea, collected between 1961 and 1994, were examined for lesions consistent with a diagnosis of TMJ-OA. Of the skulls, 913 (48.8%) were from male, 959 (51.2%) from female seals, with age at death ranging from 2 weeks to 25 years. Possible associations of TMJ-OA with dental or periodontal disorders were also analysed.ResultsLesions consistent with TMJ-OA were found in 963 (53.9%) of the 1787 juvenile/subadult (5 weeks to 5 years of age) and adult (> 5 years) specimens, the condition mostly (95.0% of affected individuals) occurring in a bilateral fashion. Males were affected more frequently than females (p < 0.001), while lesion severity tended to be higher in females (p < 0.05). Severity of TMJ-OA lesions was positively correlated with age (p < 0.001). Lesion severity was also weakly positively correlated with the number of fractured teeth (p < 0.05) and of intravitally lost teeth (p < 0.01), when controlling for age at death as a confounder.ConclusionsTMJ-OA is a common disorder in the Eastern Atlantic harbour seal. The more pronounced severity of the lesions in females compared to males is basically attributed to the higher average age of the female subsample. The causes underlying the high prevalence of TMJ-OA in the studied assemblage remain unknown. Most of the specimens (75.3%) analysed in the present study were found dead during the first phocine distemper virus epizootic in 1988. Therefore, it is assumed that, contrary to other museum collections, only little overrepresentation of pathological skeletal conditions is present in this death sample compared with the population from which it originated.