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  • Mougin, Julia, 1994, et al. (författare)
  • Fish disease prevention via microbial dysbiosis-associated biomarkers in aquaculture
  • 2022
  • Ingår i: Reviews in Aquaculture. - : Wiley. - 1753-5123 .- 1753-5131. ; 15:2, s. 579-94
  • Forskningsöversikt (refereegranskat)abstract
    • Infectious diseases are a major burden in aquaculture, and represent a significant yield-limiting factor in production that is costly to manage as well as a potential vector for zoonoses. Over the past decades, a range of new diseases have emerged, alongside increased levels of antibiotic resistance, thus heightening the need for improved disease management methods supportive of the One Health concept. Simultaneously, recent advances in Next-Generation Sequencing have increasingly elucidated the role of the microbiome in regulating metabolism, immune function and resilience. Such work has included a plethora of studies on the potential for the management of pathogens through manipulation of the microbiome, as well as related studies of the mechanisms behind host resilience. There is now an increasing robust body of evidence recognizing the importance of a holistic framework in disease aetiology between the host, its environment and colonizing microorganisms, with perturbation increasingly associated with specific dysbiotic states and disease outcomes. Elucidating disease aetiology is a preliminary step towards the development of new prevention methods, with the main goal being early identification of dysbiosis-associated biomarkers prior to any physical signs of the disease. While acknowledging the challenges associated with using key microbial taxa as biomarkers, we review recent advances in the characterization of dysbiosis and associated microbiome signatures in the context of disease development, with an emphasis on early biomarkers for aquaculture disease prevention. Several promising strategies are suggested, including the use of functional genes or metabolic pathways that are conserved between microbial taxa as a potential proxy for homeostasis.
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