Abstract

In late February 2016, a harmful algal bloom (HAB) of Alexandrium catenella was detected in southern Chiloé, leading to the banning of shellfish harvesting in an extended geographical area (~500 km). On April 24, 2016, this bloom produced a massive beaching (an accumulation on the beach surface of dead or impaired organisms which were drifted ashore) of surf clams Mesodesma donacium in Cucao Bay, Chiloé. To determine the effect of paralytic shellfish poisoning (PSP) toxins in M. donacium, samples were taken from Cucao during the third massive beaching detected on May 3, 2016. Whole tissue toxicity evidence a high interindividual variability with values which ranged from 1008 to 8763 μg STX eq 100 g−1 and with a toxin profile dominated by GTX3, GTX1, GTX2, GTX4, and neoSTX. Individuals were dissected into digestive gland (DG), foot (FT), adductor muscle (MU), and other body fractions (OBF), and histopathological and toxin analyses were carried out on the obtained fractions. Some pathological conditions were observed in gill and digestive gland of 40–50% of the individuals that correspond to hemocyte aggregation and haemocytic infiltration, respectively. The most toxic tissue was DG (2221 μg STX eq 100 g−1), followed by OBF (710 μg STX eq 100 g−1), FT (297 μg STX eq 100 g−1), and MU (314 μg STX eq 100 g−1). The observed surf clam mortality seems to have been mainly due to the desiccation caused by the incapability of the clams to burrow. Considering the available information of the monitoring program and taking into account that this episode was the first detected along the open coast of the Pacific Ocean in southern Chiloé, it is very likely that the M. donacium population from Cucao Bay has not had a recurrent exposition to A. catenella and, consequently, that it has not been subjected to high selective pressure for PSP resistance. However, more research is needed to determine the effects of PSP toxins on behavioral and physiological responses, nerve sensitivity, and genetic/molecular basis for the resistance or sensitivity of M. donacium.

Highlights

  • Paralytic shellfish poisoning (PSP) is a neurotoxic syndrome caused by the ingestion of shellfish contaminated by saxitoxin and/or its analogues, causing a range of symptoms from slight tingling sensation or numbness around the lips to fatal respiratory paralysis

  • The toxins involved in this syndrome are known to be biosynthesized by various species of marine dinoflagellates of the genera Alexandrium, Gymnodinium and Pyrodinium [2,3,4]

  • −1, which is 113 times the level considered hazardous for human consumption. This was the highest level ever recorded in this species since the monitoring program begun in 1995, This was the leveland everpersistence recorded inofthis since the monitoring program in 1995, attesting thehighest magnitude thespecies toxic A

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Summary

Introduction

Paralytic shellfish poisoning (PSP) is a neurotoxic syndrome caused by the ingestion of shellfish contaminated by saxitoxin and/or its analogues, causing a range of symptoms from slight tingling sensation or numbness around the lips to fatal respiratory paralysis (reviewed by Reference [1]). The toxins involved in this syndrome (paralytic shellfish toxins, PST) are known to be biosynthesized by various species of marine dinoflagellates of the genera Alexandrium, Gymnodinium and Pyrodinium [2,3,4]. Some HAB species could affect shellfish, with the responses depending on a series of species-specific or individual characteristics of both phytoplankton (including toxin production) and shellfish [12]. High concentrations of organisms belonging to this genus of dinoflagellates and the persistence of its blooms can produce mass mortalities of shellfish, as those reported from different geographical areas and affecting diverse bivalve species, such as mussel Mytilus meridionalis, oyster

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