No abstract

Mass mortalities due to disease outbreaks have recently affected major taxa in the oceans. For closely monitored groups like corals and marine mammals, reports of the frequency of epidemics and the number of new diseases have increased recently. A dramatic global increase in the severity of coral bleaching in 1997-98 is coincident with high El Niño temperatures. Such climate-mediated, physiological stresses may compromise host resistance and increase frequency of opportunistic diseases. Where documented, new diseases typically have emerged through host or range shifts of known pathogens. Both climate and human activities may have also accelerated global transport of species, bringing together pathogens and previously unexposed host populations. The oceans harbor enormous biodiversity by terrestrial terms (1), much of which is still poorly described taxonomically. Even less well known are the dynamics of intermittent, ephemeral, threshold phenomena such as disease outbreaks. Despite decades of intense study of the biological agents structuring natural communities, the ecological and evolutionary impact of diseases in the ocean remains unknown, even when these diseases affect economically and ecologically important species. The paucity of baseline and epidemiological information on normal disease levels in the ocean challenges our ability to assess the novelty of a recent spate of disease outbreaks and to determine the relative importance of increased pathogen transmission versus decreased host resistance in facilitating the outbreaks. Our objectives here are to review the prevalence of diseases of marine taxa to evaluate whether it can be concluded that there has been a recent increase. We also assess the contributing roles of human activity and global climate, and evaluate the role of the oceans as incubators and conveyors of human disease agents.

In January 2003, the US Environmental Protection Agency sponsored a "roundtable discussion" to develop a consensus on the relationship between eutrophication and harmful algal blooms (HABs), specifically targeting those relationships for which management actions may be appropriate. Academic, federal, and state agency representatives were in attendance. The following seven statements were unanimously adopted by attendees based on review and analysis of current as well as pertinent previous data: 1) Degraded water quality from increased nutrient pollution promotes the development and persistence of many HABs and is one of the reasons for their expansion in the U.S. and the world; 2) The composition -not just the total quantity -of the nutrient pool impacts HABs; 3) High biomass blooms must have exogenous nutrients to be sustained; 4) Both chronic and episodic nutrient delivery promote HAB development; 5) Recently developed tools and techniques are already improving the detection of some HABs, and emerging technologies are rapidly advancing toward operational status for the prediction of HABs and their toxins; 6) Experimental studies are critical to further the understanding of the role of nutrients in HAB expression, and will strengthen prediction and mitigation of HABs; and 7) Management of nutrient inputs to the watershed can lead to significant reduction in HABs. Supporting evidence and pertinent examples for each consensus statement is provided herein.

Anthropogenic activities are altering total nutrient loads to many estuaries and freshwaters, resulting in high loads not only of total nitrogen (N), but in some cases, of chemically reduced forms, notably NH 4 that promote vs. repress NO -3 uptake, assimilation, and growth in different phytoplankton groups and under different growth conditions are not well understood. Here, we review N metabolism first in a "generic" eukaryotic cell, and the contrasting metabolic pathways and regulation of NH 1 4 and NO 2 3 when these substrates are provided individually under equivalent growth conditions. Then the metabolic interactions of these substrates are described when both are provided together, emphasizing the cellular challenge of balancing nutrient acquisition with photosynthetic energy balance in dynamic environments. Conditions under which dissipatory pathways such as dissimilatory NO 2 3 / NO 2 2 reduction to NH 1 4 and photorespiration that may lead to growth suppression are highlighted. While more is known about diatoms, taxon-specific differences in NH 1 4 and NO 2 3 metabolism that may contribute to changes in phytoplankton community composition when the composition of the N pool changes are presented. These relationships have important implications for harmful algal blooms, development of nutrient criteria for management, and modeling of nutrient uptake by phytoplankton, particularly in conditions where eutrophication is increasing and the redox state of N loads is changing.

Toxic PJesteria-like dinoflagellates have been implicated as causative agent; of major fish kills (affecting IO'-10" fish) in estuaries and coastal waters of the mid-Atlantic and southeastern U.S. Transformations among an array of flagellated, amoeboid, and encysted stages in the complex life cycle of the representative species, Pjiesteria piscicida, are controlled by the availability of fresh secretions, blood, or other tissues of fish prey. P. piscicidu also is a voracious predator on other estuarine microorganisms. Pjesteria-like dinoflagellates require an unidentified substance(s) commonly found in fresh fish excreta-secreta to initiate toxin production. P. piscicida is lethal to fish at low cell densities (>250-300 cells ml-l), and at sublethal levels (-100-250 cells ml-') it has been shown to cause ulcerative fish diseases. P. piscicida also has been linked to serious human health impacts. This dinoflagellate is curythermal and euryhaline, with optima for toxic activity by the most lethal stage (toxic zoospores, TZs) at 226°C and 15 psu, respectively. Thus fdr it has shown no light optimum and :s capable of killing fish at any time during a 24-h cycle. In warmer waters (2 15°C) flagellated stages predominate while fish are dying, whereas amoebae predominate in colder conditions and when fish are dead. Nutritional stimuli influencing P. piscicida arc complex; inorganic phosphate apparently can directly stimulate TZs, whereas inorganic phosphate and nitratc indirectly promote increased production of nontoxic zoospores (NTZs, maintained in the absence of live fish, as potential precursors to lethal TZs) by stimulating their algal prey. Organic phosphate (P,) and nitrogen are taken up by P. piscicz'du osmotrophically, and P,, is stimulatory to both TZs and NTZs. The available data point to a critical need to characterize the chronic and acute impacts of toxic Pfiesteriu-like dinoflagellates on fish and other targeted prey in estuarine and coastal waters that are adversely affected by cultural eutrophication.The diverse heterotrophic dinoflagellates (Pyrrhophyta) include free-living estuarine species that demonstrate pronounced chemosensory "ambush-predator" behavior toward algal, protozoan, or fish prey (Spero and Moree 1981; Spero 1982;Ucko et al. 1989; Burkholder et al. 1995a Landsberg et al. 199.5). This behavioral pattern apparently is widespread; thus far, it has been reported from the Mediterranean Sea, the Gulf of Mexico, and the western Atlantic. In each case the feeding activity has been strikingly similar: the dinoflagellates swarm up from benthic dormant cysts when they chemically detect the prey's presence. They de- AcknowledgmentsFunding support for this research was provided by the National Science Foundation (grant OCE 94-3920) the National Sea Grant Marine Biotechnology Program, the U.S. Marine Air Station at Cherry Point/U.S. Fish & Wildlife Service (special thanks to D. Nelson and G. Hartzog), the U.S. EPA, the Neuse River Foundation, the NC Agricultural Research Foundation (project...