INVESTIGATING BLOOD LACTATE CONCENTRATION AS A PROGNOSTIC INDICATOR FOR BIRDS PRESENTING WITH BREVETOXICOSIS: 2020-2021.

Large blooms of the dinoflagellate Karenia brevis cause annual harmful algal bloom events, or "red tides" on Florida's Gulf Coast. Each year, the Clinic for the Rehabilitation of Wildlife (CROW) is presented with hundreds of cases of aquatic birds that exhibit neurologic clinical signs due to brevetoxicosis. Double-crested cormorants (Phalacrocorax auratus) are the most common species seen, and typically present with a combination of ataxia, head tremors, knuckling, and/or lagophthalmos. Blood lactate levels are known to increase in mammals for a variety of reasons, including stress, hypoxia, sepsis, and trauma, but there is limited literature on blood lactate values in avian species. The objective of this study was to determine the prognostic value of blood lactate concentration on successful rehabilitation and release of birds presenting with clinical signs consistent with brevetoxicosis. Blood lactate levels were collected on intake, the morning after presentation and initial therapy, and prior to disposition (release or euthanasia) from 194 birds (including 98 cormorants) representing 17 species during the 2020-2021 red tide season. Overall, mean blood lactate at intake, the morning after intake, and predisposition was 2.9, 2.8, and 3.2 mmol/L, respectively, for released birds across all species (2.9, 2.9, and 3.2 mmol/L for released cormorants); 3.4, 3.4, and 6.5 mmol/L for birds that died (4.0, 3.5, and 7.9 mmol/L for cormorants that died); and 3.1, 3.5, and 4.7 mmol/L for birds that were euthanized (3.5, 4.7, and 4.9 mmol/L for cormorants that were euthanized). On average, birds that died or were euthanized had an elevated lactate at all time points as compared to those that were released, but these results were not statistically significant (P = 0.13). These results indicate that blood lactate levels do not appear to be useful as a prognostic indicator for successful release of birds, including double-crested cormorants, affected by brevetoxicosis.

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

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.

Saxitoxin puffer fish poisoning in the United States, with the first report of Pyrodinium bahamense as the putative toxin source.

BACKGROUND: From January 2002 to May 2004, 28 puffer fish poisoning (PFP) cases in Florida, New Jersey, Virginia, and New York were linked to the Indian River Lagoon (IRL) in Florida. Saxitoxins (STXs) of unknown source were first identified in fillet remnants from a New Jersey PFP case in 2002. METHODS: We used the standard mouse bioassay (MBA), receptor binding assay (RBA), mouse neuroblastoma cytotoxicity assay (MNCA), Ridascreen ELISA, MIST Alert assay, HPLC, and liquid chromatography-mass spectrometry (LC-MS) to determine the presence of STX, decarbamoyl STX (dc-STX), and N-sulfocarbamoyl (B1) toxin in puffer fish tissues, clonal cultures, and natural bloom samples of Pyrodinium bahamense from the IRL. RESULTS: We found STXs in 516 IRL southern (Sphoeroides nephelus), checkered (Sphoeroides testudineus), and bandtail (Sphoeroides spengleri) puffer fish. During 36 months of monitoring, we detected STXs in skin, muscle, and viscera, with concentrations up to 22,104 microg STX equivalents (eq)/100 g tissue (action level, 80 microg STX eq/100 g tissue) in ovaries. Puffer fish tissues, clonal cultures, and natural bloom samples of P. bahamense from the IRL tested toxic in the MBA, RBA, MNCA, Ridascreen ELISA, and MIST Alert assay and positive for STX, dc-STX, and B1 toxin by HPLC and LC-MS. Skin mucus of IRL southern puffer fish captive for 1-year was highly toxic compared to Florida Gulf coast puffer fish. Therefore, we confirm puffer fish to be a hazardous reservoir of STXs in Florida's marine waters and implicate the dinoflagellate P. bahamense as the putative toxin source. CONCLUSIONS: Associated with fatal paralytic shellfish poisoning (PSP) in the Pacific but not known to be toxic in the western Atlantic, P. bahamense is an emerging public health threat. We propose characterizing this food poisoning syndrome as saxitoxin puffer fish poisoning (SPFP) to distinguish it from PFP, which is traditionally associated with tetrodotoxin, and from PSP caused by STXs in shellfish.

Brevetoxicosis: red tides and marine mammal mortalities.

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. 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. 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.