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DeCandia, A. L.

Publications and source records attributed to DeCandia, A. L..

3 recordsLinked to original sources

High retention of genomic variation and fitness-related traits in the effective population of reintroduced wolves in Yellowstone National Park

Cooperatively breeding species exhibit numerous strategies to avoid mating with close relatives, inherently reducing effective population size. For species of management concern, accurate estimates of inbreeding and trait depression are crucial for the species future. We utilized genomic and pedigree data for Yellowstone National Park gray wolves to investigate the contributions of foundation stock lineages, genetic architecture of the effective population, and putative fitness consequences of inbreeding. Our dataset spans 25 years and seven generations since reintroduction, encompassing 152 nuclear families and 329 litters. We found over 87% of the pedigree foundation genomes persisted and report influxes of allelic diversity from two translocated wolves from a divergent source in Montana. As expected for group-living species, mean kinship significantly increased over time, although we found high retention of genetic variation. Strikingly, the effective population carried a significantly lower level of genome-wide inbreeding coefficients and autozygosity with shorter decays for linkage disequilibrium relative to the non-breeding population. Lifespan and heterozygosity were higher in the effective population, although individuals who had their first litter at an older age also had higher inbreeding coefficients. Our findings highlight genetic contributions to fitness, and the importance of effective population size and gene flow to counteract loss of genetic variation in a wild, free-ranging social carnivore. It is crucial for managers to mitigate factors that significantly reduce effective population size and genetic connectivity, which supports the dispersion of genetic variation that aids in rapid evolutionary responses to environmental challenges.

evolutionary biology↗

Of Microbes and Mange: Consistent changes in the skin microbiome of three canid species infected with sarcoptic mange

Sarcoptic mange is a highly contagious skin disease caused by the ectoparasitic mite, Sarcoptes scabiei. Although it afflicts over 100 mammal species worldwide, sarcoptic mange remains a disease obscured by variability at the individual, population, and species levels. Amid this variability, it is critical to identify consistent drivers of morbidity, particularly at the skin barrier. We characterized the skin microbiome of three species of North American canids: coyotes (Canis latrans), red foxes (Vulpes vulpes), and gray foxes (Urocyon cinereoargenteus). Comparing mange-infected and uninfected individuals, we found remarkably consistent signatures of microbial dysbiosis associated with mange infection. Across genera, mange-infected canids exhibited reduced microbial diversity, altered community composition, and increased abundance of opportunistic pathogens. The primary bacteria comprising these secondary infections were Staphylococcus pseudintermedius, previously associated with canid ear and skin infections, and Corynebacterium spp, previously found among the gut flora of S. scabiei mites and hematophagous arthropods. Considered together, this evidence suggests that mange infection consistently alters the canid skin microbiome and facilitates secondary bacterial infection. These results provide valuable insights into the pathogenesis of mange at the skin barrier of North American canids and can inspire novel treatment strategies. By further adopting a \"One Health\" framework that considers mites, microbes, and the potential for interspecies transmission, we can better elucidate the patterns and processes underlying this ubiquitous and enigmatic disease.

genetics↗

Microbial dysbiosis and its implications for disease in a genetically depauperate species

THE host-associated microbiome is increasingly recognized as a critical player in health and immunity. When commensal microbial communities are disrupted, dysbiosis can contribute to disease pathogenesis and severity. Santa Catalina Island foxes (Urocyon littoralis catalinae) present an ideal case study for examining dysbiosis in wildlife due to their depauperate genomic structure and extremely high prevalence of ear canal tumors. Although the precise cause is yet unknown, infection with ear mites (Otodectes cynotis) has been linked to chronic inflammation, which is associated with abnormal cell growth and tumor development. Given the paucity of genomic variation in these foxes, other dimensions of molecular diversity, such as commensal microbes, may be critical to host response and adaptation. We therefore characterized the host-associated microbiome across six body sites of Santa Catalina Island foxes, and performed differential abundance testing between healthy and mite-infected ear canals. We found that mite infection was significantly associated with reduced microbial diversity and evenness, with the opportunistic pathogen Staphylococcus pseudintermedius dominating the ear canal community. These results suggest that secondary bacterial infection may contribute to the sustained inflammation associated with tumor development. Uncovering high abundance of S. pseudintermedius provides critical insight into the pathogenesis of this complex system, as the emergence of antibiotic resistant strains remains a concern of the medical, veterinary, and conservation communities. Through use of culture-independent sequencing techniques, this study contributes to the broader effort of applying a more inclusive understanding of molecular diversity to questions within wildlife disease ecology.

genetics↗