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Quantum computers are at the forefront of computing; however, few people understand how they work and their capabilities. We present two versions of an interactive activity designed for high school students (ages 13 to 18) that introduce a core quantum concept—entanglement. The first version illustrates a simple connection between two particles, and the second explores different ways that two particles could be entangled. This activity works well for entry-level quantum computing learning and requires minimal materials.

Stony coral tissue loss disease (SCTLD) is an emergent and often lethal coral disease that was first reported near Miami, FL (USA) in 2014. Our objective was to determine if coral colonies showing signs of SCTLD possess a specific microbial signature across five susceptible species sampled in Florida’s Coral Reef. Three sample types were collected: lesion tissue and apparently unaffected tissue of diseased colonies, and tissue of apparently healthy colonies. Using 16S rRNA high-throughput gene sequencing, our results show that, for every species, the microbial community composition of lesion tissue was significantly different from healthy colony tissue and from the unaffected tissue of diseased colonies. The lesion tissue of all but one species (Siderastrea siderea) had higher relative abundances of the order Rhodobacterales compared with other types of tissue samples, which may partly explain why S. siderea lesions often differed in appearance compared to other species. The order Clostridiales was also present at relatively high abundances in the lesion tissue of three species compared to healthy and unaffected tissues. Stress often leads to the dysbiosis of coral microbiomes and increases the abundance of opportunistic pathogens. The present study suggests that Rhodobacterales and Clostridiales likely play an important role in SCTLD.

Samples from eight species of corals (Colpophyllia natans, Dendrogyra cylindrus, Diploria labyrinthiformis, Meandrina meandrites, Montastraea cavernosa, Orbicella faveolata, Pseudodiploria strigosa, and Siderastrea siderea) that exhibited gross clinical signs of acute, subacute, or chronic tissue loss attributed to stony coral tissue loss disease (SCTLD) were collected from the Florida Reef Tract during 2016–2018 and examined histopathologically. The hallmark microscopic lesion seen in all eight species was focal to multifocal lytic necrosis (LN) originating in the gastrodermis of the basal body wall (BBW) and extending to the calicodermis, with more advanced lesions involving the surface body wall. This was accompanied by other degenerative changes in host cells such as mucocyte hypertrophy, degradation and fragmentation of gastrodermal architecture, and disintegration of the mesoglea. Zooxanthellae manifested various changes including necrosis (cytoplasmic hypereosinophilia, pyknosis); peripheral nuclear chromatin condensation; cytoplasmic vacuolation accompanied by deformation, swelling, or atrophy; swollen accumulation bodies; prominent pyrenoids; and degraded chloroplasts. Polyhedral intracytoplasmic eosinophilic periodic acid–Schiff-positive crystalline inclusion bodies (∼1–10 μm in length) were seen only in M. cavernosa and P. strigosa BBW gastrodermis in or adjacent to active lesions and some unaffected areas (without surface lesions) of diseased colonies. Coccoidlike or coccobacilloidlike structures (Gram-neutral) reminiscent of microorganisms were occasionally associated with LN lesions or seen in apparently healthy tissue of diseased colonies along with various parasites and other bacteria all considered likely secondary colonizers. Of the 82 samples showing gross lesions of SCTLD, 71 (87%) were confirmed histologically to have LN. Collectively, pathology indicates that SCTLD is the result of a disruption of host–symbiont physiology with lesions originating in the BBW leading to detachment and sloughing of tissues from the skeleton. Future investigations could focus on identifying the cause and pathogenesis of this process.

Data on Karenia brevis red tides (≥105 cells l-1) and on dead or debilitated (i.e. stranded) Kemp's ridleys Lepidochelys kempii, loggerheads Caretta caretta, green turtles Chelonia mydas, hawksbills Eretmochelys imbricata, and leatherbacks Dermochelys coriacea documented in Florida during 1986-2013 were evaluated to assess red tides as a sea turtle mortality factor. Unusually large numbers of stranded sea turtles were found coincident with red tides primarily along Florida's Gulf coast but also along a portion of Florida's Atlantic coast. These strandings were mainly adult and large immature loggerheads and Kemp's ridleys, and small immature green turtles and hawksbills. Unusually large numbers of stranded leatherbacks never coincided with red tide. For the 3 most common species, results of stranding data modeling, and of investigations that included determining brevetoxin concentrations in samples collected from stranded turtles, all indicated that red tides were associated with greater and more frequent increases in the numbers of stranded loggerheads and Kemp's ridleys than in the number of stranded green turtles. The mean annual number of stranded sea turtles attributed to K. brevis red tide was 80 (SE = 21.6, range = 2-338). Considering typical stranding probabilities, the overall mortality was probably 5-10 times greater. Red tide accounted for a substantial portion of all stranded loggerheads (7.1%) and Kemp's ridleys (17.7%), and a smaller portion of all stranded green turtles (1.6%). Even though K. brevis red tides occur naturally, the mortality they cause needs to be considered when managing these threatened and endangered species.

Coelomic fluid aspiration has been utilized in echinoderms in research and clinical settings. Detailed procedural descriptions for coelomic fluid sampling in sea urchins (class Echinoidea) are lacking, and samples are prone to contamination. The objectives of this study were to (1) standardize a technique for coelomic fluid collection in long-spined sea urchin Diadema antillarum that optimizes the diagnostic quality of the sample utilizing diagnostic imaging, (2) identify coelomic fluid bacterial isolates (using Biolog GEN III MicroLog and 16s rDNA sequencing), and (3) compare positive cultures to animal weight, holding time prior to sampling, water temperature, and gross fluid appearance. Seventy Diadema antillarum from the Florida Keys collected in two groups (March and September 2015) were utilized. Positive cultures for bacterial contamination were identified in 5% and 44%, respectively, of animals in the sampling groups. Vibrio spp. was the predominant genus identified. Positive cultures were more frequent in the group with smaller-sized animals, increased holding times, and elevated water temperatures. Deviation from clear-pink gross coelomic fluid appearance did not reliably predict bacterial contamination. A standardized technique for coelomocentesis was defined. The use of the proposed coelomocentesis methodology may facilitate improved health evaluations of sea urchins and may be applicable to research, conservation efforts, and disease investigations.

As quantum computation (QC) comes closer to reality, questions arise as to what elements to teach, how to teach it, and to what depth. QC instruction typically depends heavily on advanced math and/or physics. Our interdisciplinary science / computer science / education team co-created quantum computing (QC) learning trajectories (LT), zines, and activities, for young learners. We present the LT's (Superposition, Quantum State, Entanglement, Measurement, and Reversibility) and the iterative process that created them.

We describe a die-off of little brown bats ( Myotis lucifugus carissima) associated with acute intoxication with microcystin-LR in 2016 at Scofield Reservoir in Utah, US. High levels of this cyanotoxin in water from the reservoir and gastrointestinal content of bats supported this diagnosis.

As part of a state-wide multispecies survey of amphibian diseases, sampling was conducted at Archbold Biological Station, Venus, Florida, USA, on 15 April 2011. Gross examination of southern toad (Anaxyrus terrestris) larvae was unremarkable, but infections by a mesomycetozoean-like organism were observed in longitudinally sectioned routine haematoxylin and eosin-stained histologic slides. In 100% of the sectioned specimens examined (n = 5), a high density of the organism, representing several developmental stages, was found in the central nervous system, mainly in the spinal cord, brain, retina and optic nerve. No host inflammatory responses were found to be associated with the parasitic infection. Free, mature schizonts were occasionally found in the gill chamber and, more commonly, in the dorsal roof area. No organisms were found in other organs examined histologically, i.e. liver, kidney, heart, alimentary tract, exocrine pancreas and skeletal muscles. Presumptive mesomycetozoean ichthyophonids in anurans are usually reported to be pathogenic, especially affecting skeletal muscle tissue and causing death. To our knowledge, this is the first report of a similar organism infecting primarily the central nervous system in an amphibian.

In the summer of 2010, a sustained multispecies fish kill, affecting primarily adult red drum (Sciaenops ocellatus) and Atlantic stingray (Dasyatis sabina), along with various baitfish such as menhaden (Brevoortia spp.) and shad (Dorosoma spp.), was documented for six weeks along 50 km of the Lower St. Johns River (LSJR), Florida. An Aphanizomenon flos-aquae bloom was present in the freshwater reaches before the fish kill. The kill was triggered by a significant reverse-flow event and sudden influx of high-salinity water in late May that contributed to the collapse of the bloom upstream and brought euryhaline fish downstream into the vicinity of the senescing bloom or its by-products. The decomposing bloom led to a sequence of events, including the release of small amounts of cyanotoxins, bacterial lysis of cyanobacterial cells, high organic loading, and changes in the diversity and dominance of the plankton community to include Microcystis spp., Leptolyngbya sp., Pseudanabaena spp., Planktolyngbya spp., and low concentrations of Heterosigma akashiwo. Dissolved oxygen levels were within normal ranges in the reach of the fish kill, although elevated ammonia concentrations and high pH were detected farther upstream. These conditions resulted in complex pathological changes in fish that were not consistent with acute cyanotoxin exposure or with poor water quality but were attributable to chronic lethal hemolysis. Potential sources of hemolytic activity included H. akashiwo, Microcystis spp., and Bacillus cereus, a hemolytic bacterium. The continued presence of A. flos-aquae in the LSJR could have significant environmental repercussions and ideally the causal factors contributing to bloom growth and maintenance should be fully understood and managed.

A multispecies amphibian larval mortality event, primarily affecting American bull- frogs Lithobates catesbeianus, was investigated during April 2011 at the Mike Roess Gold Head Branch State Park, Clay County, Florida, USA. Freshly dead and moribund tadpoles had hemor- rhagic lesions around the vent and on the ventral body surface, with some exhibiting a swollen abdomen. Bullfrogs (100%), southern leopard frogs L. sphenocephalus (33.3%), and gopher frogs L. capito (100%) were infected by alveolate parasites. The intensity of infection in bullfrog livers was high. Tadpoles were evaluated for frog virus 3 (FV3) by histology and PCR. For those southern leopard frog tadpoles (n = 2) whose livers had not been obscured by alveolate spore infection, nei- ther a pathologic response nor intracytoplasmic inclusions typically associated with clinical infec- tions of FV3-like ranavirus were noted. Sequencing of a portion (496 bp) of the viral major capsid protein gene confirmed FV3-like virus in bullfrogs (n = 1, plus n = 6 pooled) and southern leopard frogs (n = 1, plus n = 4 pooled). In July 2011, young-of-the-year bullfrog tadpoles (n = 7) were neg- ative for alveolate parasites, but 1 gopher frog tadpole was positive. To our knowledge, this is the first confirmed mortality event for amphibians in Florida associated with FV3-like virus, but the extent to which the virus played a primary role is uncertain. Larval mortality was most likely caused by a combination of alveolate parasite infections, FV3-like ranavirus, and undetermined etiological factors.

In 2005 and 2006, the central west Florida coast experienced two intense Karenia brevis red tide events lasting from February 2005 through December 2005 and August 2006 through December 2006. Strandings of sea turtles were increased in the study area with 318 turtles (n = 174, 2005; n = 144, 2006) stranding between 1 January 2005 and 31 December 2006 compared to the 12-yr average of 43 +/- 23 turtles. Live turtles (n = 61) admitted for rehabilitation showed clinical signs including unresponsiveness, paresis, and circling. Testing of biological fluids and tissues for the presence of brevetoxin activity by enzyme-linked immunosorbent assay found toxin present in 93% (52 of 56) of live stranded sea turtles, and 98% (42 of 43) of dead stranded sea turtles tested. Serial plasma samples were taken from several live sea turtles during rehabilitation and toxin was cleared from the blood within 5-80 days postadmit depending upon the species tested. Among dead animals the highest brevetoxin levels were found in feces, stomach contents, and liver. The lack of significant pathological findings in the majority of animals necropsied supports toxin-related mortality.

A passive acoustic survey using a random stratified design detected spawning aggregations of sand seatrout Cynoscion arenarius over 2 sequential spawning seasons (2004 and 2005) in Tampa Bay, Florida. In 2005, an intense Karenia brevis red tide at ichthyotoxic concentra- tions entered Tampa Bay 3 mo after the spawning season began. The bloom persisted through the end of the spawning season and was temporally associated with significant changes in the spatial distribution of spawning aggregations. Red tide was most prevalent and concentrated within the lower portion of Tampa Bay and extended to a lesser degree into the middle bay, but remained absent from the upper bay. While the percentage of sand seatrout aggregations in the middle bay zone did not significantly change from 2004 to 2005, aggregations in the non-impacted area of the upper bay increased, and the red tide-exposed lower bay experienced a significant and pro- nounced decline. These significant bay-wide changes in the sand seatrout spawning population coincided with the red tide event, most notably the considerable decline in the lower bay, but the broad spatial distribution of the aggregations in concert with certain reproductive and life history characteristics may buffer the population from long-term effects. Typically, it is difficult to assess the effect of disturbances on marine fish populations due to complexities in measuring the extent of the perturbation and the magnitude of the loss to the population. Our spatially explicit sampling design further enabled us to demonstrate the widespread effects of red tide on fisheries and pro- vides an important tool for assessing the extent of loss to a spawning fish population.

Harmful algal bloom events caused by the dinoflagellate Karenia brevis occurred along the central west Florida, USA, coast from February 2005 through December 2005 and from August 2006 through December 2006. During these events, from 4 February 2005 through 28 November 2006, live, debilitated seabirds admitted for rehabilitation showed clinical signs that included disorientation, inability to stand, ataxia, and seizures. Testing of blood, biologic fluids, and tissues for brevetoxin by enzyme-linked immunosorbent assay found toxin present in 69% (n=95) of rehabilitating seabirds. Twelve of the 19 species of birds had evidence of brevetoxin exposure. Commonly affected species included Double-crested Cormorants (Phalacrocorax auritus), Brown Pelicans (Pelecanus occidentalis), Great Blue Herons (Ardea herodias), and Common Loons (Gavia immer). Serial blood and fecal samples taken from several live seabirds during rehabilitation showed that brevetoxin was cleared within 5-10 days after being admitted to the rehabilitation facility, depending on the species tested. Among seabirds that died or were euthanized, the highest brevetoxin concentrations were found in bile, stomach contents, and liver. Most dead birds had no significant pathologic findings at necropsy, thereby supporting brevetoxin-related mortality.

Table summarizing results from expert elicitation process to project the frequency and magnitude of Florida manatee mortality events caused by red tide (Karenia brevis).

Within the context of ubiquitous overfishing of piscivores, recent consequent increments of jellyfish and clupeids have occurred at the zooplanktivore trophic level in the eastern Gulf of Mexico (GOM), after overfishing of one of their predators, i.e. red snapper. Initiation of a local trophic cascade thence led to declines of herbivore stocks, documented here on the West Florida shelf. These exacerbating world-wide trophic cascades have resulted in larger harmful algal blooms (HABs), already present at the base of most coastal food webs. Impacts on human health have thus far been minimal within nutrient-rich coastal regions. To provide a setting for past morbidities, consideration is given to chronologies of other trophic cascades within eutrophic, cold water marine ecosystems of the Scotian Sea, in the Gulf of Alaska, off Southwest Africa, within the Barents, White, and Black Seas, in the Gulf of Maine, and finally in the North Sea. Next, comparison is now made here of recent ten-fold increments within Florida waters of both relatively benign and saxitoxic HABs, some of which are fatal to humans. These events are placed in a perspective of other warm shelf systems of the South China and Caribbean Seas to assess prior and possible future poison toxicities of oligotrophic coastal habitats. Past wide-spread kills of fishes and sea urchins over the Caribbean Sea and the downstream GOM are examined in relation to the potential transmission of dinoflagellate saxitoxin and other epizootic poison vectors by western boundary currents over larger “commons” than local embayments. Furthermore, since some HABs produce more potent saxitoxins upon nutrient depletion, recent decisions to ban seasonal fertilizer applications to Florida lawns may have unintended consequences. In the future, human-killing phytoplankton, rather than relatively benign fish-killing HABs of the past, may be dispersed along the southeastern United States seaboard.

An unusually persistent red tide event caused by the ichthyotoxic dinoflagellate Karenia brevis occurred along the southwest Florida coast in 2005. Extensive fish kills led to concerns regarding the effect of red tide on fish populations and their subsequent recruitment. Community structure differences were analyzed for all small- and large-bodied nekton species collected by fisheries-independent monitoring from 1996 through 2006. Indices of abundance of five economically important fish species were also calculated from this time period. A significant change in small- and large-bodied nekton community structure was apparent from summer 2005 through spring 2006. Declines in the annual recruitment of juvenile spotted seatrout (Cynoscion nebulosus), sand seatrout (Cynoscion arenarius), and red drum (Sciaenops ocellatus) were evident in 2005 and 2006. Species-specific subadult and adult abundances, however, were consistent with those of previous years. These community shifts and species-specific declines appear to be associated with the red tide event.

In October 2000, a mass mortality of blacktip sharks (Carcharhinus limbatus) and Atlantic sharpnose sharks (Rhizoprionodon terraenovae) in northwest Florida occurred in conjunction with a Karenia brevis red tide bloom. Before this incident, no information existed on red tide-induced shark mortalities or baseline brevetoxin levels in sharks and rays from red tide-endemic areas. We report here that brevetoxin accumulation in live and red tide-killed elasmobranchs is common during K. brevis blooms and non-bloom periods. Strong relationships were found between the frequency of red tide blooms and the average brevetoxin concentrations in elasmobranch tissues. The presence of brevetoxins in Atlantic coast sharks in the absence of documented K. brevis blooms may suggest that blooms are occurring in areas that are not well monitored. Although red tide-related shark mortalities are rarely observed, the presence of brevetoxins in shark embryos raises questions about the effects these toxins may have on the reproductive success of sharks.

Avian vacuolar myelinopathy (AVM) is a disease that has been reported to cause significant mortalities of birds such as bald eagles and waterfowl in the southeastern United States sinse 1994. The most likely etiological agent of AVM is a neurotoxin that originates from an unnamed toxic cyanobacterium in the Order Stigonematales. This cyanobacterium is epiphytic on submersed macrophytes. most notably hydrilla (Hydrilla verticillata). Although AVM has been documented in five other southern states, its presence in Florida has not been indicated from bird mortality events. However, the presence of the cyanobacterium had yet to be investigated despite abundant hydrilla coverage in lakes and streams. After monitoring 47 lakes and two rivers throughout Florida from November 2006 to March 2008. we positively identified the suspect cyanobacterium. both morphologically and genetically, from one lake in southcentral Florida—Lake Huntley.

Two specimens of the Caribbean spiny lobster Panulirus argus captured by lobster fishers offshore of southeast Florida, USA, between late 2007 and early 2008 had completely white abdominal muscle tissue with a 'cooked' appearance. Wet-mount examination of the skeletal muscle tissue revealed masses of microsporidian spores. Histopathology of longitudinally sectioned skeletal muscle showed that the microsporidian spores displaced much of the muscle mass, but were interspersed with small empty vacuoles (approximately 5 microm in diameter) found adjacent to necrotic skeletal muscle. Skeletal muscle showed both liquefactive and coagulative necrosis. Transmission electron microscopy of the microsporidian spores revealed characteristics--including microvilli extending from the surface of the exospore, a unikaryotic spore (width 1.0 +/- 0.13 microm, range 0.8 to 1.4 microm; length 1.4 +/- 0.11 microm, range 1.2 to 1.6 microm; mean +/- SD, N = 16), and an isofilar polar filament-consistent with the genus Ameson, which is known to infect other palinurid lobsters. Microsporidiosis in Caribbean spiny lobsters has rarely been reported within the lobster's range, with only one brief report coming from the Florida Keys in 1976. Potential risks to the lobster fishery are unknown but warrant further study.

As recently as a decade ago, Karenia brevis red tides and their effects on animal resources in the Gulf of Mexico were principally perceived as acute blooms that caused massive fish kills. Although occasional mortalities of higher vertebrates were documented, it has only been in the past decade that conclusive evidence has unequivocally demonstrated that red tides and their brevetoxins are lethal to these organisms. Brevetoxins can be transferred through the food chain and are accumulated in or transferred by biota at many trophic levels. The trophic transfer of brevetoxins in the food web is a complex phenomenon, one that is far more complicated than originally conceived. Unexplained fish kills and other animal mortalities in areas where red tide is endemic are being increasingly linked with post-bloom exposures of biota to brevetoxins. Mass mortality events of endangered Florida manatees (Trichechus manatus latirostris) follow a consistent spatial and temporal pattern, occurring primarily in the spring in southwestern Florida. Persistent blooms can also cause a cascade of environmental changes, affecting the ecosystem and causing widespread die-offs of benthic communities. Ongoing fish kills from sustained blooms can lead to short-term declines in local populations. Although animal populations in areas where red tide is endemic are unquestionably at risk, it remains to be determined to what extent populations can continue to recover from these sustained effects.

Toxic Florida red tides of the dinoflagellate Karenia brevis have downstream consequences of 500–1000 km spatial extent. Fish stocks, shellfish beds, and harmful algal blooms of similar species occupy the same continental shelf waters of the southeastern United States, amounting to economic losses of more than 25 million dollars in some years. Under the aegis of the Center for Prediction of Red tides, we are now developing coupled biophysical models of the conditions that lead to red tides and impacted coastal fisheries, from the Florida Panhandle to Cape Hatteras. Here, a nitrogen isotope budget of the coastal food web of the West Florida shelf (WFS) and the downstream South Atlantic Bight (SAB) reaffirms that diazotrophs are the initial nutrient source for onset of red tides and now identifies clupeid fish as the major recycled nutrient source for their maintenance. The recent isotope budget of WFS and SAB coastal waters during 1998–2001 indicates that since prehistoric times of Timacua Indian settlements along the Georgia coast during 1075, ∼50% of the nutrients required for large red tides of >1 μg chl l −1 of K. brevis have been derived from nitrogen-fixers, with the other half from decomposing dead sardines and herrings. During 2001, >90% of the harvest of WFS clupeids was by large ichthyotoxic red tides of >10 μg chl l −1 of K. brevis , rather than by fishermen. After onset of the usual red tides in summer of 2006 and 2007, the simulated subsequent fall exports of Florida red tides in September 2007 to North Carolina shelf waters replicate observations of just ∼1 μg chl l −1 on the WFS that year. In contrast, the earlier red tides of >10 μg chl l −1 left behind off West Florida during 2006, with less physical export, are instead 10-fold larger than those of 2007. Earlier, 55 fish kills were associated with these coastal red tides during September 2006, between Tampa and Naples. Yet, only six fish kills were reported there in September 2007. With little export of red tides and their fish prey during the former year, the computed larger nutrient-sated, fish-fed growth rates of the model’s dinoflagellates also replicate satellite-observed daily increments of K. brevis during fall maintenance in 2006, compared to simulated smaller fish-starved growth rates of decanted red tides during fall 2007. During the last few decades, K. brevis has remained a “prudent predator” of some clupeids, i.e. Spanish sardine, whereas humans have now overfished other Florida stocks of both thread herring and Atlantic shad. Thus, future operational forecasts of the land falls and durations of Florida red tides, from Louisiana to North Carolina, as well as prudent management of regional fisheries of the southeastern United States, require consideration of negelected fish losses, at intermediate trophic levels, to algal predators. Some clupeids are harvested by K. brevis , but these fish are separately supported by a longer parallel diatom-based food chain of calanoid copepods, feeding the zooplanktivores and thence other piscivore fish predators, while intersecting the shorter food chain of just diazotrophs and red tide dinoflagellates, poorly grazed in turn by harpactacoid copepods. The distinct phytoplankton functional groups, different herbivores, as well as zoophagous and piscivore fishes, must all be formulated as explicit state variables of the next set of complex ecological models, cued by satellite data and driven by nested circulation models, within an ecosystem-based management paradigm of commercial and sport harvests of biotic marine resources at higher trophic levels of the WFS and SAB.

Beginning in April 2002, three species of Florida puffer fish from around the state of Florida, USA were monitored for the presence of saxitoxin (STX). In total, 873 southern ( Sphoeroides nephelus ), 171 checkered ( S. testudineus ), and 53 bandtail ( S. spengleri ) puffer fish were collected between 2002 and 2006 from eight regions: Jacksonville, the Indian River Lagoon, Tequesta, the Florida Keys, Charlotte Harbor, Tampa Bay, Cedar Key, and Apalachicola. Emphasis was placed on collecting specimens from the Indian River Lagoon (IRL), where recreational harvesting of puffer fish led to 28 cases of saxitoxin puffer fish poisoning (SPFP) between January 2002 and May 2004. Southern puffer fish from the northern IRL routinely contained the highest concentrations of STX, with average levels in the skin of 1787 μg STXequiv./100 g tissue. Elevated concentrations were also found in the muscle (1102 μg STXequiv./100 g), gut contents (539 μg STXequiv./100 g), gonads (654 μg STXequiv./100 g), and liver (214 μg STXequiv./100 g). Lower, yet significant (above the action limit of 80 μg STXequiv./100 g tissue), concentrations of STX were also detected in the skin (599 μg STXequiv./100 g), muscle (233 μg STXequiv./100 g), gut contents (197 μg STXequiv./100 g), and gonads (239 μg STXequiv./100 g) of southern puffer fish from Tequesta in the southern IRL, as well as in the gonads (122 μg STXequiv./100 g) of Jacksonville southern puffer fish and the skin (265 μg STXequiv./100 g) of Tampa Bay southern puffer fish. STX concentrations above the action limit were also found in the skin of bandtail puffer fish from the IRL (620 μg STXequiv./100 g), Tequesta (374 μg STXequiv./100 g), and the Florida Keys (230 μg STXequiv./100 g). Checkered puffer fish collected from the IRL, Tequesta, and the Florida Keys on average were nontoxic, containing STX levels below the action limit in all tissues.

In response to multiple, unexpected cases of saxitoxin poisoning that started in January 2002, southern puffers Sphoeroides nephelus, checkered puffers S. testudineus, and bandtail puffers S. spengleri were collected from April to August 2002 from several locations in the Indian River Lagoon (IRL), Florida. Fish were analyzed for saxitoxin (STX) and tetrodotoxin (TTX) content in muscle, liver, and gonad tissues by means of the liquid chromatography-electrospray ionization-mass spectrometry method in multiple reactions monitoring mode. Spatial, species, and tissue-specific differences in toxin content and composition were found among these puffer species in the IRL. Southern puffers from the northern IRL had the highest concentrations of STX, muscle being the most contaminated tissue (1,770 ± 159 μg/100 g tissue [mean ± SD]; n = 3). Southern puffers from the Banana River and central IRL had lower amounts of STX in all tissues tested. Nearly all southern puffer tissues tested had only trace amounts...

Paralytic shellfish poisoning (PSP), due to saxitoxin and related compounds, typically results from the consumption of filter-feeding molluscan shellfish that concentrate toxins from marine dinoflagellates. In addition to these microalgal sources, saxitoxin and related compounds, referred to in this review as STXs, are also produced in freshwater cyanobacteria and have been associated with calcareous red macroalgae. STXs are transferred and bioaccumulate throughout aquatic food webs, and can be vectored to terrestrial biota, including humans. Fisheries closures and human intoxications due to STXs have been documented in several non-traditional (i.e. non-filter-feeding) vectors. These include, but are not limited to, marine gastropods, both carnivorous and grazing, crustacea, and fish that acquire STXs through toxin transfer. Often due to spatial, temporal, or a species disconnection from the primary source of STXs (bloom forming dinoflagellates), monitoring and management of such non-traditional PSP vectors has been challenging. A brief literature review is provided for filter feeding (traditional) and non-filter feeding (non-traditional) vectors of STXs with specific reference to human effects. We include several case studies pertaining to management actions to prevent PSP, as well as food poisoning incidents from STX(s) accumulation in non-traditional PSP vectors.

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.

The subjects and methodologies presented in this book vary from the presentation of a heretofore unavailable collection of data on worldwide mineral exploration to case studies of mineral exploration in the developing countries of Botswana and Papua New Guinea to a study of the economic productivity of base metal exploration in Australia and Canada. Some authors concentrate on particular actors or participants in the exploration process, such as major mining companies, while other focus on a particular country such as the Soviet Union, France, or South Africa. Most chapters deal with exploration for nonfuel minerals, and particularly metals, although some take in uranium and coal exploration; oil and gas exploration is specifically excluded.

These collected lectures offer not a design for policy, but a discussion of several issues which are central to the development of a coherent national energy policy. They include topics such as conflicting issues in policy development, and government intervention.

Puffer fish poisoning (PFP) is usually caused by ingestion of tetrodotoxins (TTXs) found naturally in certain species of puffer fish (Halstead 1967; Mosher and Fuhrmann 1984). In Japan, 20–100 people die annually from PFP, in spite of stringent controls by authorities (Ogura 1971). TTXs can cause fatal human poisoning, which is similar to paralytic shellfish poisoning (PSP) caused by saxitoxins (STXs). PSP is caused by the consumption of toxic shellfish (Shumway 1990) and rarely by fish that have have become toxic after feeding on STX-producing microalgae (Maclean 1979). As well as TTXs, STXs have also been found in at least 12 marine and freshwater puffer fish species in Asia (Ahmed et al. 2001; Kodama et al. 1983; Kungsuwan et al. 1997; Nakamura et al. 1984; Nakashima et al. 2004; Sato et al. 1997, 2000; Zaman et al. 1997), but their bioorigin has not been identified. TTXs are chemically distinct from STXs, but both neurotoxins produce similar symptoms in mammals because they act on site 1 of the voltage-dependent sodium channel, blocking the influx of sodium into excitable cells and restricting signal transmission along nerve and muscle membranes (Ahmed 1991). The symptoms of traditional PFP from TTXs and of PSP from STXs include tingling and numbness of the mouth, lips, tongue, face, and fingers; paralysis of the extremities; nausea; vomiting; ataxia; drowsiness; difficulty in speaking; progressively decreasing ventilatory efficiency; and finally in extreme cases, death by asphyxiation caused by respiratory paralysis (Ahmed 1991; Catterall 1985; Kao 1993). PFP cases in Europe (Kao 1993) and Mexico (Nunez-Vazquez et al. 2000) have occasionally been reported. In the United States, PFP has been associated with imports of puffer fish [Centers for Disease Control and Prevention (CDC) 1996]; rarely have fatalities occurred after the consumption of indigenous puffer fish. In Hawaii, white-spotted puffer fish, Arothron hispidus, were implicated in seven deaths (Ahmed 1991). Until 1974, seven PFP cases in Florida, outside of the Indian River Lagoon (IRL), were caused by the consumption of locally caught “blowfish” or puffer fish (Ahmed 1991; Benson 1956; Bigler 1999; Hemmert 1974; Mosher and Fuhrmann 1984). These cases included three fatalities, likely from TTX; for example, one woman died 45 min after consuming toxic liver from a checkered puffer fish (Sphoeroides testudineus) (Benson 1956). The toxins involved in the previous Florida PFP cases were not characterized, but because PFP is usually associated with TTX, investigators likely assumed that TTX was the cause (Benson 1956; Bigler 1999; Hemmert 1974). Tissues from Florida bandtail (Sphoeroides spengleri), checkered, and southern puffer fish (Sphoeroides nephelus) were found to be lethal in the mouse bioassay (MBA) (Burklew and Morton 1971; Lalone et al. 1963), but, again, the toxins were not determined. Until January 2002 the harvest and consumption of puffer fish from the IRL was not a risk to public health. Since then (until May 2004), however, 28 PFP cases occurring in Florida (n = 21), New Jersey (n = 3), Virginia (n = 2), and New York (n = 2) caused by puffer fish originating from the IRL were reported (Bodager 2002; CDC 2002a, 2002b). Analyses of toxins from unidentified puffer fish fillet remnants from one of the early 2002 PFP cases in New Jersey revealed STXs (Quilliam et al. 2004), not TTXs, a distinction that alone could not be made on the basis of consumer symptoms or traditional screening methods (i.e., MBA). During 2002–2004, all PFP cases were linked to puffer fish originating from the northern IRL and the Banana River on Florida’s east coast (Figure 1). Except for one case, where puffer fish were commercially harvested and reached a New Jersey fish market, puffer fish were caught recreationally [Bodager 2002; Florida Fish and Wildlife Conservation Commission (FWC) 2004]. In April 2002, state and federal officials issued health advisories, and the FWC banned puffer fish harvesting in the IRL, a ban that currently remains in effect. In New York on 14 October 2002, two PFP cases were caused from fish caught near Titusville, Florida, but frozen in March 2002 before the harvesting ban (Bodager D, personal communication). This case demonstrated the stability of toxins in puffer fish frozen for almost 9 months. Figure 1 Map showing locations (circles) in the Indian River Lagoon, Florida, where toxic puffer fish in the SPFP incidents originated (FWC 2004). Sample collections of puffer fish and Pyrodinium bahamense were conducted throughout this area and further south ... Because STXs had not previously been identified in Florida’s marine waters and their distribution, source, and origin were unknown in April 2002 (Abbott et al. 2003; Landsberg et al. 2002), we initiated an intensive survey of biota in the IRL. In this article we present a summary from 3 years of monitoring, as well as the first report of the putative toxin source.

A new genus and species of heterotrophic dinoflagellate, Cryptoperidiniopsis brodyi gen. et sp. nov., are described. This new species commonly occurs in estuaries from Florida to Maryland, and is often associated with Pfiesteria piscicida Steidinger et Burkholder, Pseudopfiesteria shumwayae (Glasgow et Burkholder) Litaker et al., and Karlodinium veneficum (Ballantine) J. Larsen, as well as other small (

Beginning in October 2000, subadult loggerhead sea turtles Caretta caretta showing clinical signs of a neurological disorder were found in waters off south Florida, USA. Histopathology indicated generalized and neurologic spirorchiidiasis. In loggerhead sea turtles (LST) with neu- rospirorchiidiasis, adult trematodes were found in the meninges of the brain and spinal cord of 7 and 3 affected turtles respectively, and multiple encephalic intravascular or perivascular eggs were asso- ciated with granulomatous or mixed leukocytic inflammation, vasculitis, edema, axonal degeneration and occasional necrosis. Adult spirorchiids were dissected from meningeal vessels of 2 of 11 LST brains and 1 of 10 spinal cords and were identified as Neospirorchis sp. Affected LST were evaluated for brevetoxins, ciguatoxins, saxitoxins, domoic acid and palytoxin. While tissues from 7 of 20 LST tested positive for brevetoxins, the levels were not considered to be in a range causing acute toxico- sis. No known natural (algal blooms) or anthropogenic (pollutant spills) stressors co-occurred with the turtle mortality. While heavy metal toxicosis and organophosphate toxicosis were also investigated as possible causes, there was no evidence for their involvement. We speculate that the clinical signs and pathologic changes seen in the affected LST resulted from combined heavy spirorchiid parasitism and possible chronic exposure to a novel toxin present in the diet of LST.

Pfiesteria shumwayae Glasgow et Burkholder is assigned to a new genus Pseudopfiesteria gen. nov. Plate tabulation differences between Pfiesteria and Pseudopfiesteria gen. nov. as well as a maximum likelihood phylogenetic analysis based on rDNA sequence data warrant creation of this new genus. The Kofoidian thecal plate formula for the new genus is Po, cp, X, 4′, 1a, 6′′, 6c, PC, 5+s, 5′′′, 0p, 2′′′′. In addition to having six precingular plates, P. shumwayae comb. nov. also has a distinctive diamond or rectangular-shaped anterior intercalary plate. Both Pfiesteria and Pseudopfiesteria gen. nov. are reassigned to the order Peridiniales based on an apical pore complex (APC) with a canal (X) plate that contacts a symmetrical 1′, four to five sulcal plates, and the conservative hypothecal tabulation of 5′′′, 0p, and 2′′′′. These morphological characters and the life histories of Pfiesteria and Pseudopfiesteria are consistent with placement of both genera in the Peridiniales. Based on the plate tabulations for P. shumwayae, P. piscicida, and the closely related “cryptoperidiniopsoid” and “lucy” groups, the family Pfiesteriaceae is amended to include species with the following tabulation: 4-5′, 0-2a, 5-6′′, 6c, PC, 5+s, 5′′′, 0p, and 2′′′′ as well as an APC containing a pore plate (Po), a closing plate (cp), and an X plate; the tabulation is expanded to increase the number of sulcal plates and to include a new plate, the peduncle cover (PC) plate. Members of the family have typical dinoflagellate life cycles characterized by a biflagellated free-living motile stage, a varying number of cyst stages, and the absence of multiple amoeboid stages.

In August and September 2001, Kuwait Bay, a semi-enclosed embayment of the Arabian Gulf, experienced a massive fish kill involving over >2500 metric tons of wild mullet ( Liza klunzingeri ), due to the bacterium Streptococcus agalactiae . In the Bay, this event was preceded by a small fish kill (100–1000 dead fish per day) of gilthead sea bream ( Sparus auratus ) in aquaculture net pens associated with a bloom of the dinoflagellate Ceratium furca . Sea bream were found to be culture positive for S. agalactiae , but did not show any visible signs of disease. Unusually warm temperatures (up to 35 °C) and calm conditions prevailed during this period. As the wild fish kill progressed, various harmful algae were observed, including Gymnodinium catenatum , Gyrodinium impudicum , and Pyrodinium bahamense var. compressum . Cell numbers of G. catenatum and G. impudicum exceeded 10 6 l −1 in some locations. All fish tested below the limits of detection for paralytic shellfish poisoning (PSP) and brevetoxins. Clams ( Circe callipyga ) were positive for PSP but at levels below regulatory limits. Nutrient concentrations, both inorganic and organic, were highly variable with time and from site to site, reflecting inputs from sewage outfalls, the aquaculture operations, a high biomass of decomposing fish, and other sources. It is hypothesized that many factors contributed to the initial outbreak of the bacterial disease, including unusual warm and calm conditions. The same factors, as well as enriched nutrient conditions, also apparently were conducive to the subsequent HAB outbreaks. The detection of PSP, while below regulatory limits, warrants further monitoring to protect human health.