Abstract

Paralytic shellfish toxins (PST) were detected in abalone (Haliotis rubra) in April 2011 in south-east Tasmania, Australia, during a dinoflagellate bloom of Gymnodinium catenatum. This led to restrictions on abalone harvesting and triggered continued PST monitoring by Ultra Performance Liquid Chromatography (UPLC-FLD) of abalone and mussels (Mytilus galloprovincialis), and concurrent phytoplankton monitoring, between 2011 and 2013. PST up to 2437 μg STX eq kg−1 (three times the bivalve regulatory limit) were confirmed in abalone viscera, with toxicity up to 586 μg STX eq kg−1 in the muscular foot (mainly doSTX and minor proportions of STX and dcSTX). Mussels accumulated PST at a faster rate than abalone which suggests they can serve as sentinels of PST accumulation to inform abalone risk management protocols.Three lines of evidence for G. catenatum as the source of PST in abalone were established: (1) PST in abalone tissues increased and declined in association with dinoflagellate blooms; (2) G. catenatum DNA was detected by real-time PCR in abalone digestive tracts; and (3) the PST analogues (toxin profile) observed in both abalone viscera and mussels were similar suggesting a common PST source. This is the first time a conclusive linkage between the occurrence of PST in abalone and a dinoflagellate source has been demonstrated.

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