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RED TIDE TOXINS POSE LINGERING THREAT TO MARINE MAMMALS Press Release June 08, 2005
As reported in the June 9 issue of Nature, scientists from the Florida Fish and Wildlife Conservation Commission’s Fish and Wildlife Research Institute (FWC/FWRI) and the University of North Carolina Wilmington Center for Marine Science (UNCW/CMS) together with collaborators from Mote Marine Laboratory, Harbor Branch Oceanographic Institution and the National Oceanographic and Atmospheric Administration (NOAA) have discovered how brevetoxin accumulation and transfer in the food web, a series of interconnected food chains, resulted in mass fatalities of endangered manatees in 2002 and bottlenose dolphins in 2004. In Florida, red tides cause massive fish kills, contaminate shellfish with brevetoxins making them unsafe for human consumption, and can cause respiratory problems in humans. Brevetoxins, the dangerous neurotoxins produced during Florida red tides (blooms of the toxic microalga Karenia brevis) also have been implicated in numerous mass marine mammal deaths in Florida. However, the mechanisms of intoxication leading to their deaths have remained uncertain. “We knew that brevetoxins were involved in manatee mortalities, but we did not understand how these herbivorous mammals could be exposed to lethal amounts of toxins after the red tide had dissipated,” said Leanne Flewelling of FWRI’s Harmful Algal Blooms group and first author of the publication.
The involvement of brevetoxins in dolphin mortalities has been much debated, primarily because toxins were not always found in dead animals and because the source of the poisoning was not understood. “Because red tides typically result in massive fish kills, people believed that brevetoxins could not accumulate to concentrations dangerous for marine mammals that feed on whole live fish prey,” said Jerome Naar, research assistant professor at UNCW/CMS and corresponding author in the publication. With funding from the Centers for Disease Control and Prevention, the Florida Department of Health and FWC, Naar, the principal investigator, and Flewelling, along with Jan Landsberg (FWC/FWRI), co-PI, Karen Steidinger (FWC/FWRI) and Daniel Baden (UNCW/CMS), all co-authors of the publication, have been studying the potential for fish to accumulate brevetoxins by food-web transfer and demonstrated that fish can be a significant source of vectored brevetoxin in the food web. They explained that planktivorous fish can in fact feed on the red tide cells, but brevetoxin seems to be fatal to them only if the toxin passes through their gills. When there is only a low level of toxin dissolved in the seawater, these fish can become contaminated, particularly in the internal organs, and can cause fatalities in other species, such as dolphin or seabirds which rely on whole fish as a food source.
“Discovering exactly the same toxin composition in the dolphin stomachs as in the planktivorous fish gave us quite a good indication of what was responsible,” Naar said. “The finding that red tide is this toxic to manatees and dolphins highlights the need for more research on the health effects of red tide toxin exposure in human populations,” said David Schwartz, M.D., director of the National Institute of Environmental Health Sciences. Despite documented annual red tides in the Gulf of Mexico since the late 1800s, there are no reports of human poisonings from fish consumption in red-tide impacted areas. The investigation of the dolphin mortality led by NOAA included multiple scientists from state and federal agencies as well as other non-profit organizations and universities. Additional funding support for the study was obtained from the Center for Sponsored Coastal Ocean Research Harmful Algal Bloom Event Response Fund, the National Institute of Environmental Health Sciences, NOAA’s Monitoring and Event Response for Harmful Algal Blooms program, and the NOAA Marine Biotoxins Program. Note to press: For high-resolution versions of the images in this article, please contact the FWRI Outreach Coordination Office at (727) 896-8626.
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