Karenia mikimotoi induced adverse impacts on abalone Haliotis discus hannai in Fujian coastal areas, China

Abstract Large-scale outbreaks of the dinoflagellate Karenia mikimotoi caused substantial mortality of abalone, Haliotis discus hannai in Fujian, China in 2012, resulting in 20 billion in economic losses to abalone industries. However, the mechanism behind the mortality, especially the reaction of abalone to this microalgal toxicity, which possibly differed significantly from the former ‘fish killer’ strain in the South China Sea (SCS). Our study revealed that K. mikimotoi FJ-strain exhibited a four-fold higher haemolytic toxicity than the SCS-strain during the late exponential phase. At the microalgal cell density of 3 × 10 7 cell L −1 , the FJ-strain caused abalone mortality of 67% in 48 h, with decreased granulocyte–hyalinocyts ratio and phagocytic activity by 58.96% and 75.64%, respectively, increased haemocyte viability by 4.8-fold and severe gill damage. The toxic effect only worked for the haemolytic toxicity from active algal cells, which were probably produced under the contact of algal cells and abalone gills. However, under exposure to the SCS-strain, more than 80% of individuals survived under aeration. The results indicated that FJ-strain was a new K. mikimotoi ecotype with stronger toxicity. It evoked severe effects, with complete abalone mortality within 24 h under the cascading effect of non-aeration (dissolved oxygen declined to 2.0 mg L −1 ), when exposed to K. mikimotoi FJ-strain at the above density. Thus, apart from the microalgal toxicity, DO depletion exacerbated the mortality of abalone in the experiment. The massive abalone mortalities in Fujian were probably caused by the combination of microalgal toxic effects and oxygen depletion, leading to immunological depression and histopathological disruption.