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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.

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.

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.

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.

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.

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.

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 (

(2002). The Effects of Harmful Algal Blooms on Aquatic Organisms. Reviews in Fisheries Science: Vol. 10, No. 2, pp. 113-390.

As anthropogenic and natural infl uences continue to exert their effects on the marine environment, the all pervasive threat of Harmful Algal Blooms (HABs) on natural resources and ecosystems becomes a more complicated issue to manage. In parallel, more effects are being documented. For example, albeit rare over 20 yr ago, more than 40% of marine mammal strandings in the USA have been attributed to HAB toxins in the last two decades (Bossart et al. 1998, Scholin et al. 2000, Van Dolah et al. 2003, Flewelling et al. 2005, Gulland and Hall 2007, Landsberg et al. 2009, Torres de la Riva et al. 2009, Fire and Van Dolah 2012, Twiner et al. 2012), and the frequency of events appears to be increasing (Gulland and Hall 2007).

Fibropapillomatosis (FP) in green turtles Chelonia mydas is a debilitating, neoplastic disease that has reached worldwide epizootic levels. The etiology of FP is unknown but has been linked to oncogenic viruses. Toxic benthic dinoflagellates (Prorocentrum spp.) are not typically considered tumorigenic agents, yet they have a worldwide distribution and produce a tumor promoter, okadaic acid (OA). Prorocentrum spp. are epiphytic on macroalgae and seagrasses that are normal components of green turtle diets. Here we show that green turtles in the Hawaiian Islands consume Prorocentrum and that high-risk FP areas are associated with areas where P. lima and P. concavum are both highly prevalent and abundant. The presence of presumptive OA in the tissues of Hawaiian green turtles further suggests exposure and a potential role for this tumor promoter in the etiology of FP.

Protistan parasites associated with a disease syndrome in tropical fish from the lower east coast of Florida to the upper Florida Keys were investigated. One of these pathogens inducing mortality in aquariumheld French angelfish Pomacanthus paru and gray angelfish Pomacanthus arcuatus is Brooklynella hostilis. This cyrtophorine ciliate was isolated from the gills and examined for the first time with scanning electron microscopy.

In the Florida Panhandle region, bottlenose dolphins (Tursiops truncatus) have been highly susceptible to large-scale unusual mortality events (UMEs) that may have been the result of exposure to blooms of the dinoflagellate Karenia brevis and its neurotoxin, brevetoxin (PbTx). Between 1999 and 2006, three bottlenose dolphin UMEs occurred in the Florida Panhandle region. The primary objective of this study was to determine if these mortality events were due to brevetoxicosis. Analysis of over 850 samples from 105 bottlenose dolphins and associated prey items were analyzed for algal toxins and have provided details on tissue distribution, pathways of trophic transfer, and spatial-temporal trends for each mortality event. In 1999/2000, 152 dolphins died following extensive K. brevis blooms and brevetoxin was detected in 52% of animals tested at concentrations up to 500 ng/g. In 2004, 105 bottlenose dolphins died in the absence of an identifiable K. brevis bloom; however, 100% of the tested animals were positive for brevetoxin at concentrations up to 29,126 ng/mL. Dolphin stomach contents frequently consisted of brevetoxin-contaminated menhaden. In addition, another potentially toxigenic algal species, Pseudo-nitzschia, was present and low levels of the neurotoxin domoic acid (DA) were detected in nearly all tested animals (89%). In 2005/2006, 90 bottlenose dolphins died that were initially coincident with high densities of K. brevis. Most (93%) of the tested animals were positive for brevetoxin at concentrations up to 2,724 ng/mL. No DA was detected in these animals despite the presence of an intense DA-producing Pseudo-nitzschia bloom. In contrast to the absence or very low levels of brevetoxins measured in live dolphins, and those stranding in the absence of a K. brevis bloom, these data, taken together with the absence of any other obvious pathology, provide strong evidence that brevetoxin was the causative agent involved in these bottlenose dolphin mortality events.

Three species of myxosporeans were found in common snook Centropomus undecimalis in Florida. One of the species is described as Myxobolus centropomi n. sp. (trophozoites in gill, pseudobranch, and under scales), and another is described as Ceratomyxa choleospora n. sp. (trophozoites and spores in gallbladder, spores in fecal casts). The third species was Fabespora sp., and its presence represents a new record and geographical location for the genus.

Based on isolations from naturally infected fish in Florida, we investigated the role of the fungi Aphanomyces invadans, Achlya bisexualis, and Phialemonium dimorphosporum in the etiology of ulcerative mycosis (UM) in striped mullet Mugil cephalus. We injected healthy striped mullet subcutaneously with secondary zoospores of four oomycete isolates: two concentrations (50 and 115 zoospores/mL) of SJR (an endemic isolate of Aphanomyces invadans in American shad Alosa sapidissima from the St. Johns River); two concentrations each of CAL (25 and 65 zoospores/mL) and ACH (1,400 and 2,000 zoospores/mL; endemic isolates of Aphanomyces invadans and Achlyva bisexualis, respectively, in striped mullet from the Caloosahatchee River); and two concentrations of the ascomycete culture MTZ (2,500 and 3,500 zoospores/mL; endemic isolate of P. dimorphosporum from whirligig mullet M. gyrans in the Matanzas Inlet). All fish injected with either concentration of SJR developed granulomatous ulcers after 8 d and died within 21 d. Eighty percent (8/10) of fish injected with the high dose of CAL developed ulcers after 13 d and died within 28 d, but only 30% (3/10) of fish injected with the low dose of CAL developed ulcers. Four of the ulcerated fish died within 28 d, and the remaining fish were terminated after 32 d. Fish injected with zoospores of Aphanomyces invadans developed ulcers that were grossly and histologically similar to those observed in naturally infected striped mullet with UM from several estuaries or rivers in Florida. These hemorrhagic skin ulcers were characterized by myonecrosis and the presence of mycotic granulomas. None of the fish injected with ACH, MTZ, or sterile water developed ulcers. This study fulfilled Koch's postulates and demonstrated that ulcers could be experimentally induced in striped mullet after exposure via injection to secondary zoospores of an endemic Florida strain of Aphanomyces invadans.

The pathogenic oomyceteAphanomyces invadansis the primary etiological agent in ulcerative mycosis, an ulcerative skin disease caused by a fungus-like agent of wild and cultured fish. We developed sensitive PCR and fluorescent peptide nucleic acid in situ hybridization (FISH) assays to detectA. invadans. Laboratory-challenged killifish (Fundulus heteroclitus) were first tested to optimize and validate the assays. Skin ulcers of Atlantic menhaden (Brevoortia tyrannus) from populations found in the Pamlico and Neuse River estuaries in North Carolina were then surveyed. Results from both assays indicated that all of the lesioned menhaden (n= 50) collected in September 2004 were positive forA. invadans. Neither the FISH assay nor the PCR assay cross-reacted with other closely related oomycetes. These results provided strong evidence thatA. invadansis the primary oomycete pathogen in ulcerative mycosis and demonstrated the utility of the assays. The FISH assay is the first molecular assay to provide unambiguous visual confirmation that hyphae in the ulcerated lesions were exclusivelyA. invadans.

Lesions in estuarine finfish are associated with a variety of organisms including parasites and bacterial, viral, and fungal infectious agents. In addition, trauma, suboptimal water quality, and other abiotic stress factors may result in the loss of homeostasis. We have observed solitary ulcerative lesions on menhaden sampled from the Chesapeake Bay, Maryland, the Pamlico River, North Carolina, and the St. Johns River, Florida. Histologically, the lesions demonstrated a marked chronic inflammatory infiltrate and granulomas in response to fungal hyphae throughout large areas of exposed necrotic muscle. Gram-negative rod-shaped bacteria were also observed in the lesions, a common finding in ulcers of aquatic organisms. Similar observations in menhaden and other species have been described previously in the literature as ulcerative mycosis, mycotic granulomatosis, red spot disease, and epizootic ulcerative syndrome. Despite the many different known causes of fish lesions, the popular press and the scientific literature have recently emphasized Pfiesteria piscicida and other Pfiesteria-like dinoflagellates (and their bioactive compounds) as the primary causative agent for finfish lesions, particularly mycotic granulomatous ulcers in Atlantic menhaden. While some laboratory data suggest that Pfiesteria may play a role in field-observed lesions, much more cause-and-effect evidence is needed to determine the importance of other risk factors, both alone or and in combination with Pfiesteria. In order to better understand the etiology of lesion initiation and progression in estuarine finfish, accurate assessments of environmental conditions collected on appropriate temporal and spatial scales, and fish morphological indicators consistent with gross and histological pathologic terminology, should be used for reporting fish lesion observations and kills. Further, this outlook will help to avoid bias and may foster a broader perspective for examining the health of estuarine systems in general.

During the 1994/1995 EMAP-Estauries program in the Carolinian Province we investigated the feasibility of using parasites of fish as response indicators. Parasites of fish are an indigenous component of healthy ecosystems. Within the EMAP-E design, the suite of environmental parameters which may affect parasite abundance, richness, prevalence, and diversity can be divided into three categories: 1) the physical and chemical characteristics of the water and sediment (including contaminants) external to the fish; 2) the internal environment defined by the physical condition (physiological) of individual fish; and 3) the presence and relative abundance of benthic macroinvertebrates, many of which serve as intermediate hosts. The biotic response of parasites to environmental stressors is also reflected in the health of fish. Parasite assemblages of silver perch Bairdiella chrysura respond to both natural and anthropogenic stressors. Our results showed that particular environmental stressors and specific parasites that respond include: temperature and monogeneans; contaminants and nematodes; low dissolved oxygen and protists; and salinity, together with a mixture of metal and organic contaminants and crustacea. Parasites of fish are useful biomarkers and appear to be more sensitive to environmental stressors than are the fish themselves. Parasite responses to selected environmental stressors may be used to discriminate polluted and unpolluted sites. The use of parasites of fish as biomarkers has relevant application to fisheries management and coastal monitoring programs.

Dinoflagellates can be classified both botanically and zoologically; however, they are typically put in the botanical division Pyrrhophyta. As a group they appear most related to the protistan ciliates and apicomplexans at the ultrastructure level. Within the Pyrrhophyta are both unarmored and armored forms of the dominant, motile flagellated stage. Unarmored dinoflagellates do not have thecal or wall plates arranged in specific series, whereas armored species have plates that vary in thickness but are specific in number and arrangement. In armored dinoflagellates, the plate pattern and tabulation is a diagnostic character at the family, subfamily, and even genus levels. In most cases, the molecular characterization of dinoflagellates confirms the taxonomy on the basis of external morphology; this has been demonstrated for several groups. Together, both genetic and morphological criteria are becoming increasingly important for the characterization, separation, and identification of dinoflagellates species. Pfiesteria and Pfiesteria-like species are thinly armored forms with motile dinospore stages characterized by their distinct plate formulae. Pfiesteria piscicida is the best-known member of the genus; however, there is at least one other species. Other genetically and morphologically related genera, now grouped under the common names of "Lucy," "Shepherd's crook," and cryptoperidiniopsoid, are being studied and described in separate works. All these other heterotrophic dinoflagellate groups, many of which are thought to be benign, co-occur in estuarine waters where Pfiesteria has been found.

Five new species of myxosporean parasite are described from cultured tilapias in Israel. These are: Myxosoma sarigi, Myxosoma equatorialis, Myxobolus israelensis, Myxobolus agolus, and Myxobolus galilaeus. The first four were found in hybrids of Oreochromis aureus X Oreochromis niloticus while Myxobolus galilaeus was found in Sarotherodon galilaeus. In addition, M. sarigi, M. israelensis, and Myxobolus sp. were also found in S. galilaeus. In the light of the present study, the taxonomy of myxosporean infections in tilapias is modified. Mature spores may localize in the melano-macrophage centers of the spleen and kidney where they may eventually be destroyed. No cases of mortality have so far been associated with these parasites.

Goussia cichlidarum n. sp. (Barrouxiidae, Apicomplexa) is a coccidian parasite found in the epithelial lining of the swimbladder in a variety of cichlid fish, most commonly inSarotherodon galilaeus. Infected fish were found in Lake Kinneret and in fish ponds in Israel and in Uganda. Natural infections were investigated as well as experimental infections obtained in the laboratory. Merogony and gamogony is completed within a hypertrophic host cell. The latter is displaced to the surface of the epithelial layer and during the parasitization process is reduced to a membranous envelope. This cell remains attached to the epithelial layer up until the stage of oogony. Oocysts complete their differentiation free in the swimbladder lumen.