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Thousands of Caspian seals (Phoca caspica) died in the Caspian Sea from April to August 2000. Lesions characteristic of morbillivirus infection were found in tissue specimens from dead seals. Canine [...]

On 9 June 2008, the UK's largest mass stranding event (MSE) of short-beaked common dolphins (Delphinus delphis) occurred in Falmouth Bay, Cornwall. At least 26 dolphins died, and a similar number was refloated/herded back to sea. On necropsy, all dolphins were in good nutritive status with empty stomachs and no evidence of known infectious disease or acute physical injury. Auditory tissues were grossly normal (26/26) but had microscopic haemorrhages (5/5) and mild otitis media (1/5) in the freshest cases. Five lactating adult dolphins, one immature male, and one immature female tested were free of harmful algal toxins and had low chemical pollutant levels. Pathological evidence of mud/seawater inhalation (11/26), local tide cycle, and the relative lack of renal myoglobinuria (26/26) suggested MSE onset on a rising tide between 06∶30 and 08∶21 hrs (9 June). Potential causes excluded or considered highly unlikely included infectious disease, gas/fat embolism, boat strike, by-catch, predator attack, foraging unusually close to shore, chemical or algal toxin exposure, abnormal weather/climatic conditions, and high-intensity acoustic inputs from seismic airgun arrays or natural sources (e.g., earthquakes). International naval exercises did occur in close proximity to the MSE with the most intense part of the exercises (including mid-frequency sonars) occurring four days before the MSE and resuming with helicopter exercises on the morning of the MSE. The MSE may therefore have been a “two-stage process” where a group of normally pelagic dolphins entered Falmouth Bay and, after 3–4 days in/around the Bay, a second acoustic/disturbance event occurred causing them to strand en masse. This spatial and temporal association with the MSE, previous associations between naval activities and cetacean MSEs, and an absence of other identifiable factors known to cause cetacean MSEs, indicates naval activity to be the most probable cause of the Falmouth Bay MSE. [ABSTRACT FROM AUTHOR]

Population genetic structure of North Atlantic killer whale samples was resolved from differences in allele frequencies of 17 microsatellite loci, mtDNA control region haplotype frequencies and for a subset of samples, using complete mitogenome sequences. Three significantly differentiated populations were identified. Differentiation based on microsatellite allele frequencies was greater between the two allopatric populations than between the two pairs of partially sympatric populations. Spatial clustering of individuals within each of these populations overlaps with the distribution of particular prey resources: herring, mackerel and tuna, which each population has been seen predating. Phylogenetic analyses using complete mitogenomes suggested two populations could have resulted from single founding events and subsequent matrilineal expansion. The third population, which was sampled at lower latitudes and lower density, consisted of maternal lineages from three highly divergent clades. Pairwise population differentiation was greater for estimates based on mtDNA control region haplotype frequencies than for estimates based on microsatellite allele frequencies, and there were no mitogenome haplotypes shared among populations. This suggests low or no female migration and that gene flow was primarily male mediated when populations spatially and temporally overlap. These results demonstrate that genetic differentiation can arise through resource specialization in the absence of physical barriers to gene flow. [ABSTRACT FROM AUTHOR]

Microbiology records for 1127 cetaceans stranded on English and Welsh beaches and examined at the Institute of Zoology between 1990 and 2019 were reviewed to identify cases of Erysipelothrix rhusiopathiae, an uncommon but potentially fatal zoonotic pathogen. Once cases were identified, prevalence was calculated, corresponding postmortem reports were reviewed, common gross and histopathological findings were identified, and antibiotic susceptibilities were determined. Overall prevalence for E. rhusiopathiae was 0.62% (7/1127; 95% CI: 0.30-1.28%). It was isolated from 3 bottlenose dolphins Tursiops truncatus, 3 harbor porpoises Phocoena phocoena, and 1 short-beaked common dolphin Delphinus delphis, with a prevalence of 21.4% (3/14; 95% CI: 7.6-47.9%), 0.39% (3/779; 95% CI: 0.13-1.13%), and 0.47% (1/212; 95% CI: 0.08-2.62%) for each species, respectively. E. rhusiopathiae resulted in septicemia in all cases from which it was isolated. Gross necropsy findings included pulmonary edema (5/7), hemorrhage (5/7) and/or congestion of various organs (4/7), and serosanguineous effusion (3/7; pericardial: 3/7, pleural: 2/6, abdominal: 2/6). Congestion (5/5), bacterial emboli (4/5), and hemorrhage (4/5) were commonly observed on histopathology, and acute renal tubular injury (2/5) and pulmonary edema (2/5) were occasionally observed. Routine bacterial cultures were vital in identifying E. rhusiopathiae, since gross lesions were often subtle and nonspecific. The liver, kidney, and brain were key organs from which E. rhusiopathiae was consistently isolated. Antibiotic resistance was uncommon and was only observed for amikacin and trimethoprim sulfonamide. Penicillins were consistently effective, along with fluoroquinolones, macrolides, clindamycin, cephalexin, and oxytetracycline.

The mammalian radiation has corresponded with rapid changes in noncoding regions of the genome, but we lack a comprehensive understanding of regulatory evolution in mammals. Here, we track the evolution of promoters and enhancers active in liver across 20 mammalian species from six diverse orders by profiling genomic enrichment of H3K27 acetylation and H3K4 trimethylation. We report that rapid evolution of enhancers is a universal feature of mammalian genomes. Most of the recently evolved enhancers arise from ancestral DNA exaptation, rather than lineage-specific expansions of repeat elements. In contrast, almost all liver promoters are partially or fully conserved across these species. Our data further reveal that recently evolved enhancers can be associated with genes under positive selection, demonstrating the power of this approach for annotating regulatory adaptations in genomic sequences. These results provide important insight into the functional genetics underpinning mammalian regulatory evolution., (Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.)