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Toxic dinoflagellates and Vibrio spp. act independently in bivalve larvae
De Rijcke, M.; Van Acker, E.; Nevejan, N.; De Schamphelaere, K.A.C.; Janssen, C.R. (2016). Toxic dinoflagellates and Vibrio spp. act independently in bivalve larvae. Fish Shellfish Immunol. 57: 236-242.
In: Fish & Shellfish Immunology. Academic Press: London; New York. ISSN 1050-4648; e-ISSN 1095-9947, meer
Peer reviewed article  

Beschikbaar in  Auteurs 

    Mytilus edulis Linnaeus, 1758 [WoRMS]; Vibrio Pacini, 1854 [WoRMS]
Author keywords
    Mytilus edulis; Harmful algae; Vibrio spp.; Phenoloxidase activity

Auteurs  Top 
  • De Schamphelaere, K.A.C., meer
  • Janssen, C.R., meer

    Harmful algal blooms (HABs) and marine pathogens – like Vibrio spp. – are increasingly common due to climate change. These stressors affect the growth, viability and development of bivalve larvae. Little is known, however, about the potential for interactions between these two concurrent stressors. While some mixed exposures have been performed with adult bivalves, no such work has been done with larvae which are generally more sensitive. This study examines whether dinoflagellates and bacteria may interactively affect the viability and immunological resilience of blue mussel Mytilus edulis larvae. Embryos were exposed to environmentally relevant concentrations (100, 500, 2500 & 12,500 cells ml−1) of a dinoflagellate (Alexandrium minutum, Alexandrium ostenfeldii, Karenia mikimotoi, Protoceratium reticulatum, Prorocentrum cordatum, P. lima or P. micans), a known pathogen (Vibrio coralliilyticus/neptunius-like isolate or Vibrio splendidus; 105 CFU ml−1), or both. After five days of exposure, significant (p < 0.05) adverse effects on larval viability and larval development were found for all dinoflagellates (except P. cordatum) and V. splendidus. Yet, despite the individual effect of each stressor, no significant interactions were found between the pathogens and harmful algae. The larval viability and the phenoloxidase innate immune system responded independently to each stressor. This independence may be related to a differential timing of the effects of HABs and pathogens.

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