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Stony coral tissue loss disease (SCTLD) was first documented in 2014 near the Port of Miami, Florida, and has since spread north and south along Florida’s Coral Reef, killing large numbers of more than 20 species of coral and leading to the functional extinction of at least one species, Dendrogyra cylindrus. SCTLD is assumed to be caused by bacteria based on presence of different molecular assemblages of bacteria in lesioned compared to apparently healthy tissues, its apparent spread among colonies, and cessation of spread of lesions in individual colonies treated with antibiotics. However, light microscopic examination of tissues of corals affected with SCTLD has not shown bacteria associated with tissue death. Rather, microscopy shows dead and dying coral cells and symbiotic dinoflagellates (endosymbionts) indicating a breakdown of host cell and endosymbiont symbiosis. It is unclear whether host cells die first leading to death of endosymbionts or vice versa. Based on microscopy, hypotheses as to possible causes of SCTLD include infectious agents not visible at the light microscopy level or toxicosis, perhaps originating from endosymbionts. To clarify this, we examined corals affected with SCTLD and apparently healthy corals using transmission electron microscopy. Endosymbionts in SCTLD-affected and apparently healthy corals consistently had varying degrees of pathology associated with elongated particles compatible in morphology with filamentous positive single-stranded RNA viruses of plants termed anisometric viral-like particles (AVLP). There was apparent progression from early to late replication of AVLP in the cytoplasm of endosymbionts adjacent to or at times within chloroplasts, with morphologic changes in chloroplasts consistent with those seen in plant cells infected by viruses. Coral host cell pathology appeared limited to massive proliferation and lysis of mucus cells. Based on these findings, we hypothesize that SCTLD is a viral disease of endosymbionts leading to coral host death. Efforts to confirm the presence of a virus associated with SCTLD through other means would be appropriate. These include showing the presence of a virus through molecular assays such as deep sequencing, attempts to grow this virus in the laboratory through culture of endosymbionts, localization of virus in tissue sections using immunohistochemistry or in situ hybridization, and experimental infection of known-virus-negative corals to replicate disease at the gross and microscopic level.

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.

During the last several decades, Florida’s Coral Reef (FCR) has been impacted by both global and local stressors that have devastated much of its living coral cover. Additionally, since 2014 FCR has experienced a lethal disease outbreak termed stony coral tissue loss disease (SCTLD). Here, we examined SCTLD spreading dynamics within and among fragmented coral colonies and quantified lesion progression rate of two intermediately susceptible species—Montastraea cavernosa and Orbicella faveolata—through induction experiments conducted in laboratory aquaria. M. cavernosa colonies showing subacute tissue loss were sequentially fragmented parallel to the lesion edge to determine whether isolated tissue that showed no tissue-loss signs, referred to as isolated apparently healthy (AH) donor fragments, would subsequently exhibit tissue loss. Additionally, AH M. cavernosa and O. faveolata fragments, referred to as recipient fragments, were placed in direct contact with the M. cavernosa donor fragments to assess incidence of new tissue-loss lesions. Finally, AH M. cavernosa donor fragments were placed in direct contact with recipient M. cavernosa and O. faveolata fragments to account for aggression from direct contact. Samples were collected for histopathology of the corals through time. Many isolated AH donor fragments developed tissue-loss lesions during the 60-day study, suggesting SCTLD may be systemic within small-sized colonies. Our results confirmed that physical contact between recipient fragments and subacute SCTLD-lesioned tissue often led to tissue loss in recipient fragments. None of the control recipient or donor fragments experienced tissue loss. Grossly, multifocal lesions started on or adjacent to the septal and costal basal body walls with tissue loss progressing across the polyp septa and coenenchyme, respectively, in both species. Histologically, initial tissue-loss lesions in both species exhibited characteristic lytic necrosis (LN) at the basal body wall of the gastrodermis. O. faveolata exhibited higher rates of lesion appearance and subsequent mortality compared to M. cavernosa, but once a lesion appeared, M. cavernosa lost tissue faster than O. faveolata. This work contributes to the growing knowledge of SCTLD dynamics and highlights the differences in lesion progression within susceptible species.

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.

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).

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...

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.

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.

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

In early August 2008, observations by divers indicated that sea fans, particularly Gorgonia ventalina, Gorgonia flabellum, and Iciligorgia schrammi, were being covered by benthic filamentous cyanobacteria. From August 2008 through January 2009 and again in April 2009, tissue samples from a targeted G. ventalina colony affected by cyanobacteria and from a nearby, apparently healthy (without cyanobacteria) control colony, were collected monthly for histopathological examination. The primary cellular response of the sea fan to overgrowth by cyanobacteria was an increase in the number of acidophilic amoebocytes (with their granular contents dispersed) that were scattered throughout the coenenchyme tissue. Necrosis of scleroblasts and zooxanthellae and infiltration of degranulated amoebocytes were observed in the sea fan surface tissues at sites overgrown with cyanobacteria. Fungal hyphae in the axial skeleton were qualitatively more prominent in cyanobacteria-affected sea fans than in controls.

Fish and invertebrate kills were reported from September to October 1996 in the Indian River, Florida, coincident with blooms of the dinoflagellate Gymnodinium pulchellum Larsen 1994. This is the first report of a bloom of this species in the Americas. Fish and invertebrate species affected were common snook (Centropomus undecimalis), striped mullet (Mugil cephalus), hardhead catfish (Arius felis), red drum (Sciaenops ocellatus), sheepshead (Archosargus probatocephalus), black drum (Pogonias cromis), blue crab (Callinectes sapidus), and shrimp (Penaeus spp.). However, Gymnodinium pulchellum has previously caused fish kills in Japan and Australia. Examination of archived phytoplankton samples from a fish kill reported in the same area of the Indian River in August 1990 confirmed the presence of high concentrations of G. pulchellum. Fish kills associated with Alexandrium monilatum and potentially Pfiesteria-like species in the Indian River also are discussed. Scanning electron microscopy provided additional morphological detail on this distinct but little-known dinoflagellate.

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.

A coccidian, Goussia centropomi n. sp., is described from the intestine of common snook Centropomus undecimalis from Florida. Merogonic and gamogonic stages are “epicellular” in the microvillous region of epithelial cell apices. Sporogony is extracellular and sporulation is exogenous. Fresh, mature oocysts are spherical (19.1 μm long × 17.6 μm wide) and have no oocyst residuum. Sporocysts are ellipsoidal (8.5 μm long × 5.6 μm wide) and have an indistinct suture line. No obvious veil covers the sporocyst. Sporozoites are thick (7.0 μm long × 2.5 μm wide) and occupy most of the sporocyst.

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.

An outbreak of amyloodiniosis in pondcultured hybrid striped bass × white bass (female Morone saxatilis × male M. chrysops) is the northernmost documented outbreak caused by an endemic source in fish of the western Atlantic. Dinospores produced by this isolate of Amyloodinium ocellatum were anteroposteriorly flattened, as contrasted with the gymnodinoid dinospores of the A. ocellatum-type species, suggesting that more than one strain or species of A. ocellatum may exist.

Red drums Sciaenops ocellatus that became infested with the copepod Caligus elongatus during rearing in seawater ponds were successfully treated with a 20-min freshwater dip after harvest and before being stocked in the wild. This treatment killed all copepods. Short-term (30min) and long-term (18-h) treatments with Copper Control, trichlorfon, and formalin were less effective than fresh water.

A revision of the genera Myxobolus and Myxosoma is presented. On the basis of Lom & Noble (1984), all species are designated as Myxobolus. A total of 444 species of Myxobolus, including three subspecies, are listed together with their hosts. All former Myxosoma species are assigned to the genus Myxobolus and those which were previously homonyms or synonyms have been assigned new names where valid. Synonyms and other species omitted from the definitive Myxobolus list are also given.

In the spring of 1998, the Florida Fish and Wildlife Research Institute received numerous reports of lesioned or ulcerated fish primarily from the St. Lucie Estuary on the southeast coast of Florida, an area known since the late 1970s for lesions of the ulcerative mycosis (UM) type. From these and archived reports, as well as others received from different areas of Florida, we documented that diseased specimens had randomly distributed skin ulcers (usually reddened or hemorrhagic) with raised irregular margins and, in some cases, deeply penetrating hyphae in the surrounding muscle tissue. Since 1998, 256 fish (comprising 18 species) with ulcerative lesions (from 15 different locations) were confirmed with hyphae in fresh squash preparation or by histological evaluation. Squash preparations revealed nonseptate, sparsely branching, thick-walled hyphae; histological sections revealed mycotic granulomas in the dermis that occasionally penetrated into the skeletal muscle. These pathological characteristics were consistent with UM caused by the oomycete Aphanomyces invadans in Southeast Asia, Japan, Australia, and the United States. For specific identification, six isolates from ulcerated fish were cultured and prepared for molecular characterization using established diagnostic methods. Ribosomal RNA gene sequence analysis identified three isolates as Aphanomyces invadans, one as the oomycete Achlya bisexualis, and two as the ascomycete Phialemonium dimorphosporum. A more extensive survey of 67 ulcerated skin samples from fish collected between 1998 and 2003 was performed using a polymerase chain reaction assay specific for Aphanomyces invadans. Of these, 26 (38.8%) samples from seven fish species and nine collection locations were positive. Confirmation of UM associated with Aphanomyces invadans represents new host records in Florida for the sheepshead Archosargus probatocephalus, striped mullet Mugil cephalus, white mullet Mugil curema, silver perch Bairdiella chrysoura, black drum Pogonias cromis, largemouth bass Micropterus salmoides, and American shad Alosa sapidissima.

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.

Unexpected brevetoxin vectors may account for deaths long after or remote from an algal bloom.

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 were found in the catfish Clarias lazera (Val.) in Israel. These species are described as: Henneguya laterocapsulata n. sp. (cyst-like trophozoites in the skin), H. suprabranchiae n. sp. (cyst-like trophozoites in the suprabranchial respiratory organs), Sphaerospora inaequalis n. sp. (spores in the lumen of the kidney tubules), Myxidium clariae n. sp. (spores in the gall bladder) and Myxobolus heterofilamentatus n. sp. (spores in the kidney, spleen, liver, suprabranchial respiratory organ, gills, heart and urinary bladder). Their taxonomic affinities to other species are discussed. ac]19860407

Ultrastructural features of the macrogamont of Goussia cichlidarum , a coccidian parasite of cichlid fish are described. Host cells derived from the swimbladder lining epithelium are reduced to membranous sacs in early gamogony. These are displaced to the surface of the epithelium, but maintain their attachment until an early stage of oogony. An elaborate junction zone between the host cell and the epithelial cells suggests a nutritive function. Immature macrogamonts are bound by a double unit membrane with only a few micropores. Intravacuolar tubules are absent. Mature macrogamonts are bound by a single unit membrane and are surrounded by an additional two envelopes. Round organelles resembling wall-forming bodies of other coccidia, reach their maximum number and differentiation in mature macrogamonts.

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.