Potent marine neurotoxins known as brevetoxins are produced by the 'red tide' dinoflagellate Karenia brevis. They kill large numbers of fish and cause illness in humans who ingest toxic filter-feeding shellfish or inhale toxic aerosols 1 . The toxins are also suspected of having been involved in events in which many manatees and dolphins died, but this has usually not been verified owing to limited confirmation of toxin exposure, unexplained intoxication mechanisms and complicating pathologies 2-4 . Here we show that fish and seagrass can accumulate high concentrations of brevetoxins and that these have acted as toxin vectors during recent deaths of dolphins and manatees, respectively. Our results challenge claims that the deleterious effects of a brevetoxin on fish (ichthyotoxicity) preclude its accumulation in live fish, and they reveal a new vector mechanism for brevetoxin spread through food webs that poses a threat to upper trophic levels.In the spring of 2002, 34 endangered Florida manatees (Trichechus manatus latirostris) died in southwest Florida, and 107 bottlenose dolphins (Tursiops truncatus) died in waters off the Florida panhandle in the spring of 2004. In both of these unusual mortality events, extensive water surveys revealed that only low concentrations of K. brevis were present.We tested for the presence of brevetoxin in the fluids and tissues of 63 of these animals (27 manatees, 36 dolphins) and found very high concentrations in the tissues of all of them (see Supplementary information accompanies this communication on Nature's website.

No abstract

Monospecific blooms of phytoplankton can disrupt pelagic communities and negatively affect human health and economies. Interspecific competition may play an important role in promoting blooms, and so we tested (1) whether the outcome of competition between the red tide dinoflagellate Karenia brevis (ex Gymnodinium breve) and 12 cooccurring phytoplankters could be explained by allelopathic effects of compounds released by K. brevis and (2) whether waterborne, lipophilic molecules, including brevetoxins, are involved. Nine of 12 phytoplankton species were suppressed when grown with live K. brevis at bloom concentrations. K. brevis extracellular filtrates or lipophilic extracts of filtrates inhibited six of these nine species, indicating allelopathy. However, these inhibitory effects were weaker than those experienced by competitors exposed to live K. brevis. Brevetoxins at ecologically reasonable waterborne concentrations accounted for the modest inhibition by K. brevis of only one competitor, Skeletonema costatum. The addition of brevetoxins also caused significant autoinhibition, reducing the maximum concentration of K. brevis. Allelopathy is one mechanism by which K. brevis appears to exhibit competitive advantage over some sympatric phytoplankters, although unidentified compounds other than brevetoxins must be involved, in most cases. K. brevis was also susceptible to competitive exclusion by several species, including Odontella aurita and Prorocentrum minimum, known to thrive during K. brevis blooms. Although field experiments are required to assess whether allelopathy plays a fundamental role in bloom dynamics, our results indicate that allelopathy occurs widely but with species-specific consequences.Competition is one of the dominant forces structuring communities, including marine pelagic communities (Hutchinson 1961). The production and release of compounds that inhibit competitors, a process known as allelopathy, is a mechanism of interference competition that is hypothesized to be important among phytoplankton (Smayda 1997), affecting species succession (Keating 1977), especially under eutrophic conditions (Maestrini and Bonin 1981). Allelopathy may be a successful strategy for phytoplankton species that occur in dense blooms, maximizing the concentration of allelopathic compound(s) exposed to competitors and mini-1 Corresponding author (julia.kubanek@biology.gatech.edu). AcknowledgmentsThis research was supported by NSF grant OCE-0134843 to J.K. M.K.H. was supported as a summer undergraduate research assistant by the Camille and Henry Dreyfus Foundation Environmental Chemistry Program. Nutrient analyses were funded by NOAA MERHAB grant MER 02-627A to T.A.V., and ELISA analyses were funded by COP-NOAA MERHAB, NIEHS PO1 ES10594-03, and the CDC-FDOH U50/CCU423360-01 to J.N. We thank P. Tester, R. Pierce, M. Hay, and E. Litchman for advice in planning experiments and two anonymous reviewers for suggestions that improved the manuscript. We also thank E. Prince, A. Prusak, E. John, D. Collins, and A....

This paper reviews the literature describing research performed over the past decade on the known and possible exposures and human health effects associated with Florida red tides. These harmful algal blooms are caused by the dinoflagellate, Karenia brevis, and similar organisms, all of which produce a suite of natural toxins known as brevetoxins. Florida red tide research has benefited from a consistently funded, long term research program, that has allowed an interdisciplinary team of researchers to focus their attention on this specific environmental issue—one that is critically important to Gulf of Mexico and other coastal communities. This long-term interdisciplinary approach has allowed the team to engage the local community, identify measures to protect public health, take emerging technologies into the field, forge advances in natural products chemistry, and develop a valuable pharmaceutical product. The Review includes a brief discussion of the Florida red tide organisms and their toxins, and then focuses on the effects of these toxins on animals and humans, including how these effects predict what we might expect to see in exposed people.

No abstract