Brevetoxins, like ciguatoxins, are potent ichthyotoxic neurotoxins that accumulate in fish

Abstract

Brevetoxins and ciguatoxins are closely related potent marine neurotoxins. Although ciguatoxins accumulate in fish to levels that are dangerous for human consumption, live fish have not been considered as potential sources of brevetoxin exposure in humans. Here we show that, analogous to ciguatoxins, brevetoxins can accumulate in live fish by dietary transfer. We experimentally identify two pathways leading to brevetoxin-contaminated omnivorous and planktivorous fish. Fish fed with toxic shellfish and Karenia brevis cultures remained healthy and accumulated high brevetoxin levels in their tissues (up to 2675 ng g −1 in viscera and 1540 ng g −1 in muscle).Repeated collections of fish from St. Joseph Bay in the Florida panhandle reveal that accumulation of brevetoxins in healthy fish occurs in the wild. We observed that levels of brevetoxins in the muscle of fish at all trophic levels rise significantly, but not to dangerous levels, during a K. brevis bloom. Concentrations were highest in fish liver and stomach contents, and increased during and immediately following the bloom. The persistence of brevetoxins in the fish food web was followed for 1 year after the K. brevis bloom.

Prevalence of brevetoxins in prey fish of bottlenose dolphins in Sarasota Bay, Florida

“…These values are also comparable to those reported in stomach contents of Fire et al 2007). These data support previous work demonstrating that the ichthyotoxic effects of brevetoxin do not preclude its accumulation in live fish (Flewelling et al 2005, Naar et al 2007) and suggest that fish are potential vectors of brevetoxins to upper trophic levels.…”

“…The levels of brevetoxin detected in viscera of spot and pinfish (mean = 1982 and 1313 ng PbTx-3 eq g -1 , respectively) are comparable to reported concentrations detected in fish caught live (> 300 ng g -1 in spot viscera; > 400 ng g -1 in pinfish viscera) from St. Joseph Bay during the 2004 dolphin mortality event (Flewelling et al 2005) and in fish from a subsequent followup study in St. Joseph Bay (386 ng g -1 , spot; 1453 ng g -1 , pinfish) (Naar et al 2007). These values are also comparable to those reported in stomach contents of Fire et al 2007).…”

“…The present study demonstrates that, similar to fish from the St. Joseph Bay area (Flewelling et al 2005, Naar et al 2007, primary prey fish of Sarasota Bay dolphins can accumulate high concentrations of brevetoxins during Karenia brevis blooms. Fish collected in the absence of K. brevis blooms also contain detectable levels of brevetoxins, and the present study is the first to quantify non-bloom concentrations of brevetoxins in Sarasota Bay fish.…”

“…Lipophilic molecules like brevetoxin can bioaccumulate in fish (Bottein Dechraoui et al 2007) and are generally eliminated much more slowly than other hydrophilic harmful algal toxins (Landsberg 2002). Brevetoxins are detectable in experimentally and naturally exposed shellfish and finfish several weeks to several months post-exposure , Pierce et al 2006, Hinton & Ramsdell 2008 and in some cases over 1 yr post-bloom (Naar et al 2007). In southwest Florida, seagrasses also appear to have persistent detectable levels of brevetoxin in the absence of K. brevis blooms (L. J. Flewelling unpubl.…”

Effects of Karenia brevis red tide on the spatial distribution of spawning aggregations of sand seatrout Cynoscion arenarius in Tampa Bay, Florida

“…Fish kills usually originate with the lysis of K. brevis cells and the subsequent release of brevetoxins, potent neurotoxic ichthyotoxins that are absorbed directly across the gill membranes (Abbott et al 1975, Baden 1989. Kills also result from ingestion of toxic cells, water, or vectored prey (Tester et al 2000, Landsberg 2002, Naar et al 2007, Landsberg et al 2009). Neurotoxicity causes lack of muscle coordination, paralysis, convulsions, and, eventually, death by respiratory failure (Baden 1989, Landsberg 2002.…”