MEPS 505:81-94 (2014)  -  DOI: https://doi.org/10.3354/meps10793

ABSTRACT: Harmful algal blooms (HABs) caused by the dinoflagellate Cochlodinium polykrikoides have increased in geographic extent, frequency, and duration in coastal areas worldwide. These blooms have negatively impacted many coastal fisheries, causing mass mortalities of both wild and farmed fish. Forage fish species may be particularly susceptible to HABs as they feed on plankton and are highly abundant in coastal ecosystems where these blooms occur. While mortalities associated with HABs have been well documented for juvenile and adult fish, the potential impacts to early life stages (i.e. embryos and eleutheroembryos) have not been explored. We conducted a series of toxicity experiments using a clonal laboratory culture of C. polykrikoides and 3 forage fish species (Atlantic silverside Menidia menidia, inland silverside M. beryllina, and sheepshead minnow Cyprinodon variegatus) all common on the US East Coast. Our experiments demonstrated that C. polykrikoides caused mortalities in both embryos and eleutheroembryos, but that sensitivity to acute toxicity differed among fish species (M. beryllina > M. menidia > C. variegatus) and among life stages (eleutheroembryos > embryos). Although embryos were somewhat resistant to C. polykrikoides biotoxins until they hatched, once they hatched, they experienced rapid mortality and impaired swimming ability. By testing ecologically relevant exposure times to C. polykrikoides, we found that eleutheroembryos can become incapacitated relatively quickly (i.e. within hours), and that surviving fish could recover swimming ability following removal from C. polykrikoides exposure. This research provides the first evidence of sublethal impacts on fish exposed to C. polykrikoides, and advances understanding of the potential ecosystem impacts of this harmful alga.

KEY WORDS: Cochlodinium polykrikoides · Cyprinodon variegatus · Early life history · Forage fish · Harmful algal bloom · Menidia beryllina · Menidia menidia · Toxicity