Microbial communities of oysters - implications for immune status and disease

Timothy Green*, Julien de Lorgeril, Agnes Vergnes, & Caroline Montagnani
 
IFREMER, Macquarie University and the Sydney Institute of Marine Science, Chowder Bay Road, Mossman, NSW 2088, Australia

Massive mortality events of Pacific oysters (Crassostrea gigas) have been recently reported worldwide and these disease events are often associated with with Ostreid herpesvirus type 1 (OsHV-1).  Epidemiological field studies have also reported oyster age and other pathogens of the Vibrio genus are contributing factors to the disease.  We undertook a controlled laboratory experiment to simultaneously investigate survival and immunological response of juvenile and adult C. gigas at different time-points post-inoculation with OsHV-1, Vibrio splendidus and V. aestuaranius.  Our data corroborates epidemiological studies that juveniles are more susceptible to OsHV-1, whereas adults are more susceptible to Vibrio.  Interestingly, epidemiological studies often report higher mortality levels than we observed using our laboratory infection model.  However, cumulative mortality may not be a true indicator of OsHV-1 pathogenicity.  We observed a proportion of oysters inoculated with OsHV-1 become paralysed (gaping, non-responsive to external stimuli).  We measured the expression of 102 immune-genes by high-throughput RT-qPCR, which revealed oysters have different transcriptional responses to OsHV-1 and Vibrio infection.  The transcriptional response in the early stages of OsHV-1 infection involved genes related to apoptosis and the interferon-pathway.  Whereas, transcriptional response to Vibrio infection involved antimicrobial peptides, heat shock proteins and galectins.  Interestingly, oysters in the later stages of OsHV-1 infection had a transcriptional response that resembled an antibacterial response, which is suggestive of the oyster's microbiome causing secondary infections.  This study provides insights into the molecular basis for the mortality events.  Discrepancy in mortality between laboratory and field trials may reflect the antiviral response against OsHV-1 causing C. gigas to become paralysed, thus exacerbating mortality from predation, desiccation (low-tide) and secondary infections (dysbiosis).