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Abstract Since the reintroduction of African swine fever virus (ASFV) in Europe in 2007 and its subsequent spread to Asia, wild boar has played a crucial role in maintaining and disseminating the virus. There are significant gaps in the knowledge regarding infection dynamics and disease pathogenesis in domestic pigs and wild boar, particularly at the early infection stage. We aimed to compare domestic pigs and wild boar infected intranasally to mimic natural infection with one of the original highly virulent genotype II ASFV isolates (Armenia 2007). The study involved euthanising three domestic pigs and three wild boar on days 1, 2, 3, and 5 post-infection, while four domestic pigs and four wild boar were monitored until they reached a humane endpoint. The parameters assessed included clinical signs, macroscopic lesions, viremia levels, tissue viral load, and virus shedding in nasal and rectal swabs from day 1 post-infection. Compared with domestic pigs, wild boar were more susceptible to ASFV, with a shorter incubation period and earlier onset of clinical signs. While wild boar reached a humane endpoint earlier than domestic pigs did, the macroscopic lesions were comparatively less severe. In addition, wild boar had earlier viremia, and the virus was also detected earlier in tissues. The medial retropharyngeal lymph nodes were identified as key portals for ASFV infection in both subspecies. No viral genome was detected in nasal or rectal swabs until shortly before reaching the humane endpoint in both domestic pigs and wild boar, suggesting limited virus shedding in acute infections.

Harbour porpoises (Phocoena phocoena) are the only cetacean residents found year-round in Swedish waters and they are exposed to numerous natural and anthropogenic threats. Since the in situ monitoring of cetaceans can be difficult, invasive and often expensive, investigation of stranding patterns and examination of stranded animals can be used as a cost-effective source of data to study these elusive animals. The aim of this study was to investigate the spatiotemporal patterns of harbour porpoise stranding reports and the possible underlying causes in Swedish waters over a ten-year period (2014–2023). Additionally, the Swedish stranding network plays a key role in the collection of stranded carcasses for health and disease surveillance, and geographic coverage of the network also was analysed. When making spatial comparisons, the ten-year period was divided into two five-year blocks. Data on 854 stranded harbour porpoises were analysed from the coasts of the Skagerrak, Kattegat, and Baltic Seas. Both significant spatial and temporal patterns could be identified. Strandings peaked in July through September and hotspots occurred along most of the Swedish west coast, with the most frequent hotspots located around Öresund and especially the area around the Kullen peninsula. The spatial patterns of strandings found in this study are consistent with data on porpoise abundance, prey abundance, and gillnet fisheries’ efforts. The latter is known to be one of the primary causes of porpoise mortality. Furthermore, the coverage of the Swedish stranding network increased between the two periods, likely reflecting an increased awareness of the carcass-based surveillance program, and gaps requiring network expansion efforts were identified. These results also provide baseline data to enable the continued monitoring of stranding trends, as changes may indicate changes in population distribution, size or mortality rates.

Abstract In 2020/2021, several European brown hare syndrome virus (EBHSV) outbreaks were recorded in European hares (Lepus europaeus) from Catalonia, Spain. Recombination analysis combined with phylogenetic reconstruction and estimation of genetic distances of the complete coding sequences revealed that 5 strains were recombinants. The recombination breakpoint is located within the non-structural protein 2C-like RNA helicase (nucleotide position ~ 1889). For the genomic fragment upstream of the breakpoint, a non-pathogenic EBHSV-related strain (hare calicivirus, HaCV; GII.2) was the most closely related sequence; for the rest of the genome, the most similar strains were the European brown hare syndrome virus (EBHSV) strains recovered from the same 2020/2021 outbreaks, suggesting a recent origin. While the functional impact of the atypical recombination breakpoint remains undetermined, the novel recombinant strain was detected in different European brown hare populations from Catalonia, located 20–100 km apart, and seems to have caused a fatal disease both in juvenile and adult animals, confirming its viability and ability to spread and establish infection. This is the first report of a recombination event involving HaCV and EBHSV and, despite the recombination with a non-pathogenic strain, it appears to be associated with mortality in European brown hares, which warrants close monitoring.

Abstract Background In recent years, the wildlife/livestock interface has attracted increased attention due to disease transmission between wild and domestic animal populations. The ongoing spread of African swine fever (ASF) in European wild boar (Sus scrofa) emphasize the need for further understanding of the wildlife/livestock interface to prevent disease spill-over between the wild and domestic populations. Although wild boar may also act as a potential source for other infectious disease agents, ASF is currently the most severe threat from wild boar to domestic pigs. To gather information on the wild boar situation at commercial pig producing farms in Sweden, a digital questionnaire survey was distributed through the animal health services. Results Most pigs produced for commercial purposes in Sweden are raised without outdoor access. Of the 211 responding pig producers, 80% saw wild boar or signs of wild boar activity in the vicinity of their farm at least once during the year. Observations were significantly correlated with geographical region, but there was no correlation between farm characteristics (farm size, main type of production, outdoor access) and observed wild boar presence or proximity. However, a reported higher frequency of wild boar observations was positively correlated with the observations being made in closer proximity to the farm. Hunting and strategic baiting were the most common mitigation strategies used to keep wild boar at bay. Of the 14 farms raising pigs with outdoor access, 12 responded that these pigs could be raised solely indoors if needed. Pigs with outdoor access are required to be fenced in, but double fencing in these outdoor pig enclosures was not practiced by all. A perimeter fence surrounding any type of pig farm was very rare. More than half of the producers that grew crops with intended use for pigs reported crop damage by wild boar. Conclusion This study shows that although pigs raised for commercial purposes in Sweden are, to a large extent, kept indoors the potential for indirect contact with wild boar exists and must be considered. Variable local situations regarding wild boar abundance may require an adaptive approach regarding biosecurity efforts.

Europe and, more recently, the Americas are experiencing unprecedented mortality in wild and domestic birds because of the highly pathogenic avian influenza virus (HPAI) A(H5N1) virus clade 2.3.4.4b (1). Infections [...]

We found highly pathogenic avian influenza A(H5N1) virus clade 2.3.4.4b associated with meningoencephalitis in a stranded harbor porpoise (Phocoena phocoena). The virus was closely related to strains responsible for a concurrent avian influenza outbreak in wild birds. This case highlights the potential risk for virus spillover to mammalian hosts.

Drawing on our experience co-teaching an undergraduate unit called "Gender and Environment," we argue for an expansive feminist approach to teaching climate change that embodies the content of the unit in its classroom practice. This requires: (a) understanding the classroom not as separate from the phenomenon of climate change but as one of its sites, striated by the diverse bodies, histories, and other materialities that comprise it; (b) a rigorous understanding of climate change as a feminist issue, inseparable from crises of colonialism, white supremacy, patriarchal power, and violent body normativities; and (c) a commitment to responsive and accountable pedagogies. Here, the feminist environmental humanities concept and method of "composting" (Hamilton & Neimanis, 2018) helps describe how environmental matters can be mulched together with key social justice concepts and insights in order to nourish new possibilities for climate change pedagogies. Composting thus becomes a metaphoric guide for how we configure the work of teaching climate change--"not" as masterful dissemination of privileged knowledge but as a co-worlded pedagogy that learns from intersectional, anticolonial, queer, and crip perspectives. This pedagogy thus also contributes to growing more accountable and responsive feminisms within and beyond the classroom. The first half of this article explores how an understanding of both climate change and composting manifest in the context of our co-taught unit. In the second half, we offer a scrapbook--produced with care and joy but necessarily condensed and incomplete--that exemplifies some of the ways that we put this framing into practice.

Increased numbers of human infections with Chlamydia psittaci have been associated with bird feeding activities in southern Sweden. Information on occurrence and genotype of C. psittaci in garden birds in Sweden is required to corroborate this finding but data are limited. Additionally, pathogenicity of C. psittaci for garden birds is poorly understood. In this study, C. psittaci infection was investigated in 275 garden birds representing 22 species submitted for wildlife disease surveillance between 2009 and 2019. PCR was used to detect C. psittaci DNA in liver and lung. Positive samples were genotyped, additional PCR was performed on feces, and tissues were examined microscopically. C. psittaci was found in six (2.2 %) birds; three great tits (Parus major), two feral (Columba livia) and one wood pigeon (Columba palumbus). Two great tits and the wood pigeon had inflammatory lesions associated with C. psittaci. In the great tits and wood pigeon, C. psittaci genotype A, the cause of most human cases, was detected. Genotype B, considered endemic in pigeons, was detected in the feral pigeons. Low incidence of C. psittaci in dead Swedish garden birds was similar to studies on apparently healthy Swedish birds. Pathological findings were consistent with C. psittaci being fatal in half of the positive birds, which also had higher bacterial loads in feces. This highlights the risk for human infection via infected garden birds, especially regarding great tits and pigeons.

Natural cases of zooanthroponotic transmission of SARS-CoV-2 to animals have been reported during the COVID-19 pandemic, including to free-ranging white-tailed deer (Odocoileus virginianus) in North America and farmed American mink (Neovison vison) on multiple continents. To understand the potential for angiotensin-converting enzyme 2 (ACE2)-mediated viral tropism we characterised the distribution of ACE2 receptors in the respiratory and intestinal tissues of a selection of wild and semi-domesticated mammals including artiodactyls (cervids, bovids, camelids, suids and hippopotamus), mustelid and phocid species using immunohistochemistry. Expression of the ACE2 receptor was detected in the bronchial or bronchiolar epithelium of several European and Asiatic deer species, Bactrian camel (Camelus bactrianus), European badger (Meles meles), stoat (Mustela erminea), hippopotamus (Hippopotamus amphibious), harbor seal (Phoca vitulina), and hooded seal (Cystophora cristata). Further receptor mapping in the nasal turbinates and trachea revealed sparse ACE2 receptor expression in the mucosal epithelial cells and occasional occurrence in the submucosal glandular epithelium of Western roe deer (Capreolus capreolus), moose (Alces alces alces), and alpaca (Vicunga pacos). Only the European badger and stoat expressed high levels of ACE2 receptor in the nasal mucosal epithelium, which could suggest high susceptibility to ACE2-mediated respiratory infection. Expression of ACE2 receptor in the intestinal cells was ubiquitous across multiple taxa examined. Our results demonstrate the potential for ACE2-mediated viral infection in a selection of wild mammals and highlight the intra-taxon variability of ACE2 receptor expression, which might influence host susceptibility and infection.

In contrast to sparse historical observational records, five Sowerby’s beaked whales (SBW) stranded and died in Swedish waters between 2015 and 2020. Here we summarize historical records of SBWs in the Skagerrak basin and adjacent waters. The three recent stranding events from Sweden are described, and the post-mortem findings, including diet analysis, from the five SBWs are presented. Of 30 historical records of SBWs observations since 1869, 13 (43%) were documented between 2010 and 2021, and records between July and November were the most frequent. The recent stranding events occurred in October 2015 (n = 1), August 2019 (n = 3) and July 2020 (n = 1). Four of the SBWs were examined through necropsy, and one was sampled in the field. They were all sub-adults and included a single female and four males. The causes of death were emaciation, euthanasia due to traumatic injury, and live stranding of undetermined cause. Two SBWs each had a focal bone lesion consistent with osteomyelitis. Other findings included pox-like dermatitis, trauma, focal granulomas in a lymph node and intestine, and ulceration of the stomach. CT scans were performed on the heads of two animals, with inconclusive results. Three SBWs had hard parts in the gastrointestinal tract that mainly consisted of otoliths from several fish species. An eDNA-analysis confirmed and supplemented the diet analysis, revealing 17 fish species in total, including species not previously described as prey for SBW, such as Pleuronectidae spp. The apparent increase in observational records since 2010 may indicate a shift in SBW distribution or changing threats to these animals. Our results support and expand theories on SBW movements and provide data on the biology and health of this poorly known species, which are valuable for conservation and legislation efforts.

Abstract A type of monophasic group B Salmonella enterica with the antigenic formula 4,12:a:- (“Fulica-like”) has been described as associated with harbour porpoises (Phocoena phocoena), most frequently recovered from lung samples. In the present study, lung tissue samples from 47 porpoises found along the Swedish coast or as bycatch in fishing nets were analysed, two of which were positive for S. enterica. Pneumonia due to the infection was considered the likely cause of death for one of the two animals. The recovered isolates were whole genome sequenced and found to belong to sequence type (ST) 416 and to be closely related to ST416/ST417 porpoise isolates from UK waters as determined by core-genome MLST. Serovars Bispebjerg, Fulica and Abortusequi were identified as distantly related to the porpoise isolates, but no close relatives from other host species were found. All ST416/417 isolates had extensive loss of function mutations in key Salmonella pathogenicity islands, but carried accessory genetic elements associated with extraintestinal infection such as iron uptake systems. Gene ontology and pathway analysis revealed reduced secondary metabolic capabilities and loss of function in terms of signalling and response to environmental cues, consistent with adaptation for the extraintestinal niche. A classification system based on machine learning identified ST416/417 as more invasive than classical gastrointestinal serovars. Genome analysis results are thus consistent with ST416/417 as a host-adapted and extraintestinal clonal population of S. enterica, which while found in porpoises without associated pathology can also cause severe opportunistic infections.

Autoethnography and Feminist Theory at the Water's Edge: Unsettled Islands Sonja Boon, Lesley Butler, and Daze Jefferies Palgrave Pivot, 2018, viii + 146 pp. ISBN 9783319908281, $69.99 hardcover. Autoethnography and [...]

Harbour porpoises (Phocoena phocoena) are useful indicators of the health of their wild populations and marine ecosystems, yet their elusive nature makes studying them in their natural environment challenging. Stranded porpoises provide an excellent source of data to study the health and biology of these animals and identify causes of death, diseases and other threats. The aim of this study was to document pathology, and where possible, cause of death in porpoises from Swedish waters. Post-mortem examinations were performed on 128 stranded porpoises collected from 2006 to 2020. Overall, bycatch including definitive and probable cases was the most common cause of death (31.4%), followed by disease (21.3%), predominantly pneumonia. In adults, infectious disease was the most common cause of death. Bacteria with zoonotic potential such as Erysipelothrix rhusiopathiae and Brucella sp. were documented for the first time in porpoises from Swedish waters, as was the porpoise-adapted group B Salmonella enterica ST416/ST417. Three of four deaths from non-infectious diseases involved parturition complications. Four cases of suspected predation were documented, but further analyses are required to confirm these findings. Our results are consistent with those from other regions in Europe and serve as a reference for future monitoring for changing patterns of health and disease of porpoises and their environments.

Abstract Background Prior to 2010, the lagoviruses that cause rabbit hemorrhagic disease (RHD) in European rabbits (Oryctolagus cuniculus) and European brown hare syndrome (EBHS) in hares (Lepus spp.) were generally genus-specific. However, in 2010, rabbit hemorrhagic disease virus 2 (RHDV2), also known as Lagovirus europaeus GI.2, emerged and had the distinguishing ability to cause disease in both rabbits and certain hare species. The mountain hare (Lepus timidus) is native to Sweden and is susceptible to European brown hare syndrome virus (EBHSV), also called Lagovirus europaeus GII.1. While most mountain hare populations are found on the mainland, isolated populations also exist on islands. Here we investigate a mortality event in mountain hares on the small island of Hallands Väderö where other leporid species, including rabbits, are absent. Results Post-mortem and microscopic examination of three mountain hare carcasses collected from early November 2016 to mid-March 2017 revealed acute hepatic necrosis consistent with pathogenic lagovirus infection. Using immunohistochemistry, lagoviral capsid antigen was visualized within lesions, both in hepatocytes and macrophages. Genotyping and immunotyping of the virus independently confirmed infection with L. europaeus GI.2, not GII.1. Phylogenetic analyses of the vp60 gene grouped mountain hare strains together with a rabbit strain from an outbreak of GI.2 in July 2016, collected approximately 50 km away on the mainland. Conclusions This is the first documented infection of GI.2 in mountain hares and further expands the host range of GI.2. Lesions and tissue distribution mimic those of GII.1 in mountain hares. The virus was most likely initially introduced from a concurrent, large-scale GI.2 outbreak in rabbits on the adjacent mainland, providing another example of how readily this virus can spread. The mortality event in mountain hares lasted for at least 4.5 months in the absence of rabbits, which would have required virus circulation among mountain hares, environmental persistence and/or multiple introductions. This marks the fourth Lepus species that can succumb to GI.2 infection, suggesting that susceptibility to GI.2 may be common in Lepus species. Measures to minimize the spread of GI.2 to vulnerable Lepus populations therefore are prudent.

Abstract Lagovirus europaeus GI.2, also known as RHDV2 or RHDVb, is an emerging virus that causes rabbit haemorrhagic disease (RHD) in European rabbits (Oryctolagus cuniculus). In contrast to L. europaeus GI.1 (or RHDV/RHDVa) viruses that are only pathogenic for adults, GI.2 causes clinical disease in both adults and kittens. However, detailed descriptions of the pathology of this virus that may provide insight into its pathogenicity and emergence are lacking. Using an Australian GI.2 field strain isolated in 2015, we provide the first detailed description of pathology, viral antigen distribution and tissue load of GI.2 in adult and 5-week old New Zealand white rabbits using histology, immunohistochemistry and RT-qPCR. Liver was the target organ, but in contrast to GI.1 viruses, lesions and inflammatory responses did not differ between adults and kittens. Lymphocytic inflammation, proposed to be protective in kittens infected with GI.1, was notably absent. We also present the first descriptions of bone marrow changes in RHD, including decreased myeloid-to-erythroid ratio. Consistent with other pathogenic lagoviruses, intracellular viral antigen was demonstrated in hepatocytes and cells of the mononuclear phagocytic system. In terminal stages of disease, viral loads were highest in liver, serum and spleen. Despite the small sample size, our data suggest that unlike early European GI.2 strains, the pathogenicity of the Australian GI.2 virus is similar to GI.1 viruses. Additionally, GI.2 was fatal for all (n = 5) inoculated kittens in this study. This may significantly alter RHD epidemiology in the field, and may impact biocontrol programs for invasive rabbits in Australia where GI.1 viruses are intentionally released.

Introduction: Patients with hemophilia A treated with coagulation Factor VIII (FVIII) products are at risk for developing anti‐FVIII antibodies. The ABIRISK Consortium aimed to provide knowledge on the formation and detection of anti‐drug antibodies against biopharmaceutical products, including FVIII. Accordingly, standardized and validated assays for the detection of binding (total) and neutralizing antibodies are needed. Aim: Two‐center validation of an ELISA for the detection of total FVIII‐binding IgG‐antibodies and Nijmegen‐Bethesda assays for the quantification of FVIII‐neutralizing antibodies according to consensus validation guidelines. Methods: Validation of assays at both sites was done according to published recommendations and included preanalytics, the determination of key assay parameters, including cut‐points, assay sensitivity, precision, and FVIII interference. Results: The validated assays reproducibly detected FVIII‐binding and ‐neutralizing antibodies with comparable performance in both laboratories. Floating screening cut‐points were established for both assays. Determined mass‐based sensitivity of both assays (all values ≤66 ng/mL) complied with the minimum sensitivity for the detection of anti‐drug antibodies as recommended by the FDA (<100 ng/mL). Intra‐ and inter‐assay coefficients of variation did not exceed 25%. Assay validation further revealed that pre‐analytical heat treatment led to potentially false‐positive ELISA results, while up to 0.15 IU/mL, residual FVIII showed no significant impact. Overall, good agreement of results was found for patient samples analyzed at both study sites. Conclusion: Comprehensive validation of different anti‐FVIII‐antibody assays in two laboratories gave novel insights into the impact of pre‐analytical sample treatment as well as the comparability of test results generated by the use of methodically different assays. [ABSTRACT FROM AUTHOR]