Abstract

The multifactorial etiology of massive Crassostrea gigas summer mortalities results from complex interactions between oysters, opportunistic pathogens and environmental factors. In a field survey conducted in 2014 in the Mediterranean Thau Lagoon (France), we evidenced that the development of the toxic dinoflagellate Alexandrium catenella, which produces paralytic shellfish toxins (PSTs), was concomitant with the accumulation of PSTs in oyster flesh and the occurrence of C. gigas mortalities. In order to investigate the possible role of toxic algae in this complex disease, we experimentally infected C. gigas oyster juveniles with Vibrio tasmaniensis strain LGP32, a strain associated with oyster summer mortalities, after oysters were exposed to Alexandrium catenella. Exposure of oysters to A. catenella significantly increased the susceptibility of oysters to V. tasmaniensis LGP32. On the contrary, exposure to the non-toxic dinoflagellate Alexandrium tamarense or to the haptophyte Tisochrysis lutea used as a foraging alga did not increase susceptibility to V. tasmaniensis LGP32. This study shows for the first time that A. catenella increases the susceptibility of Crassostrea gigas to pathogenic vibrios. Therefore, in addition to complex environmental factors explaining the mass mortalities of bivalve mollusks, feeding on neurotoxic dinoflagellates should now be considered as an environmental factor that potentially increases the severity of oyster mortality events.

Highlights

  • The mortality of the juvenile pacific oyster Crassostrea gigas is the result of complex interactions between oysters, their environment and opportunistic pathogens

  • We earlier showed that this toxic dinoflagellate induces the apoptosis of C. gigas hemocytes at paralytic shellfish toxins (PSTs) concentrations similar to those generally observed in situ during a bloom of toxic algae [53]

  • Apoptosis was observed 24 h after exposure to A. catenella, which corresponds to the time we used for oyster infection in our experiment

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Summary

Introduction

The mortality of the juvenile pacific oyster Crassostrea gigas is the result of complex interactions between oysters, their environment and opportunistic pathogens. C. gigas oysters, like other bivalve mollusks, are filter feeders that feed on micro-phytoplankton, including toxic dinoflagellates Among these dinoflagellates, Alexandrium catenella, a paralytic shellfish toxin (PST) producer, is observed worldwide [24]. Alexandrium catenella, a paralytic shellfish toxin (PST) producer, is observed worldwide [24] Extensive blooms of this species have been reported in various marine environments, such as the Pacific Ocean of North America [25], Chile [26], New Zealand [27], Japan, China, South Korea [28,29] and the western Mediterranean Sea [30,31]. In agreement with our field observations, controlled experiments showed that an exposure of C. gigas to A. catenella significantly impacts the survival of these mollusks when further infected with the pathogenic V. tasmaniensis strain LGP32

Results
Exposure to Alexandrium catenella Increases Oyster Mortality
PSTs Accumulate in Infected Oysters
Discussion
Collection of Environmental Samples and Processing
Dynamics of Alexandrium catenella
Oyster Mortality
Oyster Biotoxin Contamination
Algae Production
Pathogenic Bacterial Strain
Experimental Design
Neurotoxins Analysis
Statistical Analysis

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