Abstract

Pacific Oyster Mortality Syndrome (POMS) affects Crassostrea gigas oysters worldwide and causes important economic losses. Disease dynamic was recently deciphered and revealed a multiple and progressive infection caused by the Ostreid herpesvirus OsHV-1 μVar, triggering an immunosuppression followed by microbiota destabilization and bacteraemia by opportunistic bacterial pathogens. However, it remains unknown if microbiota might participate to protect oysters against POMS, and if microbiota characteristics might be predictive of oyster mortalities. To tackle this issue, we transferred full-sib progenies of resistant and susceptible oyster families from hatchery to the field during a period in favor of POMS. After 5 days of transplantation, oysters from each family were either sampled for individual microbiota analyses using 16S rRNA gene-metabarcoding or transferred into facilities to record their survival using controlled condition. As expected, all oysters from susceptible families died, and all oysters from the resistant family survived. Quantification of OsHV-1 and bacteria showed that 5 days of transplantation were long enough to contaminate oysters by POMS, but not for entering the pathogenesis process. Thus, it was possible to compare microbiota characteristics between resistant and susceptible oysters families at the early steps of infection. Strikingly, we found that microbiota evenness and abundances of Cyanobacteria (Subsection III, family I), Mycoplasmataceae, Rhodobacteraceae, and Rhodospirillaceae were significantly different between resistant and susceptible oyster families. We concluded that these microbiota characteristics might predict oyster mortalities.

Highlights

  • The farmed oyster Crassostrea gigas is heavily affected by the Pacific Oyster Mortality Syndrome (POMS) targeting juveniles (Barbosa Solomieu et al, 2015; Pernet et al, 2016)

  • Holistic molecular approaches revealed the mechanism of POMS

  • These studies showed that an infection by the Ostreid herpesvirus (OsHV-1 μVar) is the critical step in the infectious process leading to an immune-compromised state by altering hemocyte physiology

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Summary

Introduction

The farmed oyster Crassostrea gigas is heavily affected by the Pacific Oyster Mortality Syndrome (POMS) targeting juveniles (Barbosa Solomieu et al, 2015; Pernet et al, 2016). Holistic molecular approaches revealed the mechanism of POMS (de Lorgeril et al, 2018; Rubio et al, 2019) These studies showed that an infection by the Ostreid herpesvirus (OsHV-1 μVar) is the critical step in the infectious process leading to an immune-compromised state by altering hemocyte physiology. This first process is followed by a microbiota destabilization which “opens the door” to bacterial pathogens (e.g., vibrios) that target hemocytes to induce their lysis. The infectious process is completed with subsequent bacteraemia, which is the ultimate step inducing oyster death

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