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Page 59 3 Harmful Algal Blooms Blooms of the single cell algae known as phytoplankton are sometimes called red tides, which have been recognized since biblical times. The phytoplankton may become so numerous that they cause the water to become discolored (i.e., red, reddish brown, green, yellow green) and these events are associated with shellfish toxicity and fish kills. Over the past twenty years, phytoplankton researchers (Anderson, 1989; Hallegraeff, 1993; Smayda, 1990; Steidinger and Baden, 1984) have noted an increasing frequency of harmful phytoplankton blooms worldwide. Of the roughly 5,000 phytoplankton species, fewer than 80 are known to be toxic, but once established, some toxic or nuisance blooms may persist because their toxins may inhibit the growth of other phytoplankton or reduce grazing pressure by zooplankton (Turner and Tester, 1989; 1997; Turner et al., 1998). The blue-green algae, or cyanobacteria, are represented by only a few marine genera, but these organisms may pose significant threats worldwide to human health in freshwater systems. The ramifications of harmful/toxic phytoplankton blooms are extensive. The loss of human life and risk of adverse health outcomes are of primary concern. Physicians and public health officials are not always trained to recognize the symptoms of poisoning from exposure to algal toxins. Regional economies are impacted when shellfish resources are tainted and cannot be harvested; mass mortality of finfish and loss of environmental quality result in further economic losses. Marine mammal deaths are linked to the concentration of several phycotoxins within marine food chains, (Bossart et al., 1998; Geraci et al., 1989) and the impact of toxic phytoplankton on non-commercial species can only be conjectured. The toxic materials produced by harmful algae are ''environmental chemicals," toxins that interfere with human and animal metabolism, nerve conduction,

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Page 60 and central nervous system processing of information. Our understanding of the mechanisms of algal intoxication depends upon the use of model animal systems, while public health monitoring of seafood and seawater provides information relevant to the health of marine species. For humans, harmful algal blooms cause illness through several routes of exposure. Toxins produced by the algae may contaminate seafood and water, or in some cases become airborne in sea spray. Of the natural marine environmental contaminants that are health risks, harmful algal blooms (HABs) are most prominent. Harmful Algal Bloom Hazards in Food Filter-feeding bivalve molluscs accumulate and concentrate phycotoxins that can be further bioconcentrated as they move through the food chain to top carnivores (Shumway 1990). Human intoxication follows ingestion of tainted shellfish or, in the case of ciguatera, finfish. The severity of symptoms is dependent upon the amount of toxin ingested, the weight and general health of the individuals, and their susceptibility to the toxin. General clinical symptoms of fish and shellfish poisoning include nausea, vomiting, abdominal pain, and diarrhea. Phycotoxins have a high affinity for specific receptor sites leading to critical changes in intracellular ion concentrations of sodium, calcium, or potassium. Consequently, action potential and nerve transmission impulses are affected. HABs are responsible for six different types of seafood poisoning, several of which can be lethal (Table 3-1). Five of these types of seafood poisoning are found in North America on a recurring basis. From 1978 to 1987, more than half of the cases of illness from naturally occurring seafood toxins were the result of harmful algal blooms toxins (IOM, 1991). The first step in determining the public health hazard from an algal bloom is identification of the species and the toxin. This has been especially problematic with Pfiesteria, where the alga is identified by electron microscopy, exposure is hard to measure because the toxin appears to be inhaled as an aerosol, and the toxin has not yet been purified and characterized, apparently because the compound is chemically unstable. Paralytic shellfish poisoning (PSP) occurs from Alaska to Mexico and from Prince Edward Island to Massachusetts. Most often, the toxins are accumulated in bivalve shellfish, but instances of accumulation in mackerel and in carnivorous gastropods have been demonstrated. Neurotoxic shellfish poisoning (NSP) is a hazard in all coastal regions of the Gulf of Mexico and at times on the Atlantic coast as far north as the Carolinas. The NSP toxins accumulate predominantly in shellfish, but recent instances of human intoxication due to consumption of toxic mullet implicates finfish in accumulation (Baden, 1998). Amnesic shellfish poisoning (ASP) causes human illness from Washington State to southern California and on Prince Edward Island. On several occasions, ASP has been documented to accumulate in anchovies; therefore, fish transvection routes to humans must be considered. Diarrheic shellfish poisoning (DSP) has been documented in

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Page 61 TABLE 3-1 Intoxication Syndromes Caused by Marine Toxins Consumed in Seafood Disease PSP NSP ASP DSP Ciguatera Puffer Fish Causative Organism Red Tide Dinoflagellate Red Tide Dinoflagellate Red Tide Diatom Red Tide Dinoflagellate Epibenthic Dinoflagellate Bacteria? Major Transvector Shellfish Shellfish Shellfish Shellfish Fish Fish Geographic Distribution Temperate to Tropical Worldwide Gulf of Mexico, Japan, New Zealand Canada, NW U.S. Temperate Worldwide Sub-Tropical to Tropical Worldwide Japan, Worldwide Major Toxin (Number) Saxitoxin (18+) Brevetoxin (10+) Domoic Acid (3) Okadaic Acid (4) Ciguatoxin (8+) Scaritoxin, Maitotoxin Tetrodotoxin (3+) Neuro-Mechanism Na+ Channel Blocker Na+ Channel Activator Glutamate Receptor Agonist Phosphorylase Phosphatase Inhibitor NA+, Ca2+, Channel Activators Na+ Channel Blocker Incubation Time 5–30 min 30 min-3 hr hours hours hours 5–30 min Duration days days years days years days Acute Symptoms n,v,d p,r n,v,d, b, t, p n,v,d,a, p,r d, n,v n,v,d, t, p n,v,d,p,r, bp Chronic Symptoms none none amnesia none paraesthesias none Fatality Rate 1–14% 0% 3% 0% <1% 60% Diagnosis clinical, mouse bioassay of food, HPLC clinical, mouse bioassay of food, ELISA clinical, mouse bioassay of food, HPLC clinical, mouse bioassay, HPLC, ELISA (0.1–12%) clinical, mouse bioassay, immunoassay clinical, mouse bioassay, Fluorescence Therapy Supportive (respiratory) Supportive Supportive (respiratory) Supportive Mannitol TCA? Supportive Supportive (respiratory) Prevention red tide and seafood surveillance, report cases red tide, then seafood surveillance, report cases seafood surveillance, report cases seafood surveillance, some red tide, report cases seafood surveillance, report cases (clusters) regulated food preparation, report cases PSP = Paralytic Shellfish Poisoning, NSP = Neurotoxic Shellfish Poisoning, ASP = Amnesic Shellfish Poisoning, DSP = Diarrheic Shellfish Poisoning, Ciguatera (CFP) = Ciguatera Fish Poisoning, Puffer Fish poisoning = Fugu; n = nausea, v = vomiting, d = diarrhea, p = paraesthesias, r = respiratory depression, b = bronchoconstriction, t = reversal of temperature sensation, a = amnesia, bp = decreased blood pressure. Symptoms in bold indicate pathognomonic symptoms, numbers in () indicate # of natural derivatives (from Baden et al., 1995).

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Page 62 Nova Scotia but is not a current public health problem in the United States. It must, however, be considered as a potential emerging threat in the future. Ciguatera fish poisoning (CFP) is the most common type of seafood poisoning and occurs in virtually all tropical reef regions. International transport of seafood continues to threaten public health and recent implementation of the Hazard Analysis Critical Control Point (HACCP) program by the U.S. Food and Drug Administration (FDA) seeks to address the emerging threat. This program, which was first implemented by General Foods to safeguard foods on space missions, has as its hallmark an identification of all points in a food process whereby its safety or wholesomeness can be compromised. Identification is followed by implementation of strategies to protect or preserve the integrity of the food source. Paralytic Shellfish Poisoning (PSP) Paralytic shellfish poisoning is caused by the ingestion of saxitoxin or its derivatives. Saxitoxin was first characterized in 1957 (Schantz et al., 1957) and now includes 21 recognized forms. Each of the known derivatives binds specifically (although with variable affinity) to the voltage-gated sodium channel. These toxins are water-soluble and act primarily on the peripheral nervous system and secondarily on the central nervous system. The onset of symptoms is rapid: gastrointestinal distress, tingling, numbness, and ataxia are typical. Some of the clinically diagnosed individuals die of respiratory failure. As long as medical records have been maintained, human poisoning from eating bivalves has been reported (Shantz, 1984). PSP was recognized by Native Americans before the arrival of European explorers. Several members of Capt. George Vancouver's crew succumbed to PSP while they explored the Pacific Northwest in 1798. Although the toxin is initially accumulated by shellfish, marine mammal deaths have resulted from food chain concentration in mackerel following an unusual temporal passage from red tide to thread herring (Geraci et al., 1989). Examples of cells containing saxitoxins are Alexandrium catenella, A. tamaense, Gymnodinium catenatum, and Pyrodinium bahamense var. compressum. These species represent sub-Arctic to tropical forms, and most produce cysts or resting stages triggered by temperature or other environmental changes (Anderson et al., 1983). This adaptive strategy also promotes the expansion of PSP blooms from one geographic region to another. Cysts are remarkably resilient and survive transport in ships' ballast water, in the digestive tracts of spat oysters shipped from one region to another, and are sediment-stable for years. Changes in ocean circulation patterns, disturbance of resting cyst populations, and dredging operations can move seed beds of resting cysts to new regions which may be conducive to growth. Until 1970, PSP was known only in the temperate waters of North America, Europe, and Japan; by 1990, PSP was documented in South Africa, South America, the Philippines, Australia, and India (Hallegraeff,

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Page 63 1993). At present, one dinoflagellate species responsible for PSP, P. bahamense, is confined to tropical coastal waters of the Atlantic and Indo-Pacific, however, a survey of its fossil cysts indicates a much wider geographic range in the past (Hallegraeff, 1993). Neurotoxic Shellfish Poisoning (NSP) Neurotoxic shellfish poisoning is caused by the ingestion of brevetoxin and its twelve different toxic forms. All brevetoxins bind to the voltage-gated sodium channel (Poli et al., 1986) and have the opposite effect of saxitoxin. Instead of acting like a plug on the channel, they act like a door stop and hold sodium channels in their open configuration (Jeglitsch et al., 1998). Uncontrolled nerve impulses result, ultimately leading to respiratory inhibition. Whereas saxitoxin blocks sodium transport, brevetoxin allows unregulated sodium transport. NSP produces gastrointestinal and neurological symptoms, less severe, but similar to those of ciguatera fish poisoning (see below). Blooms of Gymnodinium breve, the dinoflagellate responsible for NSP, are usually marked by large patches of discolored water and massive fish kills. In addition, this unarmored dinoflagellate can be ruptured easily by wave action, whereupon its toxins become aerosolized and cause respiratory asthma-like symptoms. G. breve red tides were documented as early as 1844 and their correlation with shellfish toxicity was recognized by 1880. However the identification and chemical characterization of the first of 10 brevetoxins was not completed until 1981, when toxin purification techniques became available (Lin et al., 1981). Toxin structures quickly followed for several other natural brevetoxins. Historically, the distribution of G. breve blooms has been in the Gulf of Mexico, with isolated occurrences recorded along Florida's east coast. However, during the fall and winter of 1987–88 there was a large, persistent G. breve bloom in the coastal waters of North Carolina, a range extension of 800–900 km for this species (Tester et al., 1989). Forty-eight cases of NSP were documented and more than $24 million dollars was lost to the local economy when many shellfish harvesting areas were closed for the entire season (Tester and Fowler, 1990). Subsequently, an explanation for this unusual event was uncovered when this dinoflagellate was found in low but consistent numbers in the Gulf Stream (Tester et al., 1991). The shoreward intrusion of warm water from meanders of the Gulf Stream, seen in Plate VIII, transported G. breve to the nearshore waters of North Carolina. In 1996, following an extensive Florida red tide, over 150 West India manatees died as a result of toxin exposure (Bossart et al., 1998). Other toxic species related to G. breve are known to cause fish kills, shore bird deaths, and shellfish toxicity in Japan, New Zealand, and possibly South Africa. The Japanese and New Zealand species produce toxins similar to brevetoxin.

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Page 64 Ciguatera Fish Poisoning (CFP) Ciguatera fish poisoning is an operational term that includes all lipid-soluble toxins that accumulate in tropical reef fish flesh, which when consumed lead to a debilitating disease characterized by reversal of temperature sensation, chronic pain and numbness in the extremities, joint and bone pain. In severe cases, these symptoms are known to persist for weeks to months and, in a few isolated cases, neurological symptoms have persisted for several years. In other cases, patients have experienced a recurrence of neurological symptoms months to years after recovery (U.S. FDA, 1997). Several ciguatoxins have been isolated and a variety of other toxins are thought to contribute to the syndrome. Ciguatoxin, isolated from Pacific moray eel tissue, binds to the same site of voltage gated sodium channels as does brevetoxin. CFP was first recognized in the 1550s in the Caribbean (Martyr and Novo, 1912), but the causative agent was not identified until the mid-1980s (Carmichael et al., 1986; ILO, 1984; Sakamoto et al., 1987). CFP has a pantropical distribution between 34 S and 35 N and is known from the Caribbean basin, Florida, the Hawaiian Islands, French Polynesia, and Australia (Anderson and Lobel, 1987). It has been associated with a suite of at least 6 toxins produced by a multispecies assemblage of benthic, (sessile, epiphytic) dinoflagellates, including Gambierdiscus toxicus, some Prorocentrums, Ostreopsis, and Coolia. Ciguatoxin structures resemble brevetoxin, and their molecular mechanism of action is identical. These toxins are bioconcentrated by higher carnivores, especially reef fish, which may remain toxic for more than 2 years after becoming contaminated (Helfrich et al., 1968). There is mounting evidence that Pacific and Caribbean ciguatera toxins are different chemical entities and many investigators believe there are some elusive toxins within the "ciguatera" operational definition that have not yet been isolated. Worldwide, 50,000 victims are stricken annually (Bomber and Aikman, 1988/89) with CFP; cases per thousand residents vary between 3–9 in the Caribbean to 5–13 in French Polynesia. It is estimated that only 20–40% of the cases are reported. In the acute phase of CFP, gastrointestinal distress is followed by neurological and cardiovascular symptoms that can be, but rarely are, fatal. A chronic phase can persist for weeks, months, or years (Freudenthal, 1990). There is no antidote to CFP and supportive therapy is the rule. In extreme cases of CFP, death through respiratory paralysis may occur within 2–24 hours of ingestion. Repeated exposure to ciguatoxins exacerbates the symptoms, therefore, CFP is considered a major health and economic problem in many tropical islands where fish is a large part of the diet. CFP is one of the most important constraints to fisheries resources development in these regions (Olsen et al., 1984) and also poses a threat to uninformed tourists (Freudenthal, 1990). CFP accounts for over half of all seafood intoxication (IOM, 1991)

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Page 65 Diarrheic Shellfish Poisoning (DSP) Diarrheic shellfish poisoning is due to the consumption of okadaic acid and two related derivatives. Unlike the toxins that interact with nerve channel proteins, this toxin group inhibits protein phosphatases, a group of enzymes responsible for smooth muscle function, for regulation of cell division in vertebrates, and for overall phosphate metabolism. Diarrhea and tumor promotion are two toxic effects ascribed to okadaic acid. DSP was first reported from Japan in 1976, (Yasumoto et al., 1980) where okadaic acid produced by several species of the dinoflagellate Dinophysis and Prorocentrum was found to be the cause. DSP is not fatal, recovery is within three days with or without medical treatment and its symptoms are easily mistaken for bacterial gastric infections. Over a 5-year period (1976–1982), 1,300 DSP cases were reported in Japan; in 1981 5,000+ cases were reported in Spain; in 1983 3,300+ cases were reported in France (Hallegraeff, 1993). DSP has been documented in Japan, Europe, Chile, Thailand, and New Zealand, but prior to 1990 DSP was not known to occur in North or South America. Then, in 1990 and 1992, DSP occurred along the southern coast of Nova Scotia (Quilliam et al., 1993). DSP was also documented in Uruguay in 1992 (Mendez, 1992). Some consider DSP to be the most widespread phytotoxin-caused seafood illness. This is particularly significant because of recent findings indicating that okadaic acid is mutagenic (Anune and Undestad, 1993). Although DSP-producing species of phytoplankton occur throughout all temperate coastal waters of the United States, no outbreaks of DSP have been documented in U.S. waters. Amnesic Shellfish Poisoning (ASP) Amnesic shellfish poisoning is due to the accumulation of domoic acid by shellfish. Domoic acid binds to a specific subset of glutamic acid brain receptors known as the kainate receptor. Normally, this receptor, in part, functions in establishing short- and long-term memory. Impaired, intoxicated individuals can die if the dose is sufficient or experience permanently impaired memory function. ASP was recognized for the first time in 1987 on Prince Edward Island when over 100 acute cases and 4 deaths resulted from consumption of blue mussels (Bates et al., 1989). Subsequent studies of this illness revealed that the neurotoxin domoic acid, produced by a diatom, Pseudo-nitzschia multiseries, caused the ASP outbreak. Typical symptoms of severe cases include gastroenteritis followed by dizziness, headache, seizures, disorientation, short-term memory loss, and respiratory difficulty. In the Bay of Fundy, generally two blooms of Pseudo-nitzschia occur each year; one when the water temperature warms to about 10 ¹C and the second occurs

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Page 66 later, following the highest water temperatures of the year in late August (Martin et al., 1993). Despite the annual blooms of the diatoms that cause ASP in Canadian waters, contaminated shellfish have been kept off the market by vigilant management practices. Hence, public confidence in the local mussel industry is high; mussel harvests there now exceed the 1987 levels (Wood and Shapiro, 1993). In the fall of 1991, domoic acid was detected in dead sea birds in Monterey Bay, California. They had been feeding on anchovies that had ingested Pseudo-nitzschia australis, another source of domoic acid. Further tests found domoic acid present in razor clams and crabs from Oregon and Washington; subsequently, both recreational and commercial fisheries were closed (Wood and Shapiro, 1993). As recently as May 21–31, 1998, the death of 50 California sea lions in the Monterey area was caused by domoic acid. Although no known human intoxication resulted from either of these incidents, it was a clear warning that domoic acid can accumulate in marine food chains. Cyanotoxins Cyanotoxins (i.e., alkaloid neurotoxins, hepatotoxins) are produced by some species (or strains) of all the common freshwater genera of blue-green algae, also known as cyanobacteria (e.g., Anabena, Aphaanizomenon, Microcystis, Nodularia, Nostoc, Oscillatoria) (Carmichael, 1992) and several species of marine cyanobacteria, including Trichodesmium thiebautii (Guo and Tester, 1994; Hawser et al., 1991). These cyanotoxins produce intermittent but repeated cases of animal poisonings in many areas of the world. Poisoning cases, known since the late 19th century, involve sickness and death of livestock, pets, and wildlife following ingestion of water containing toxic algae or the toxin(s) released by the aging cells (Charmichael, 1992). No acute lethal poisoning of humans by consuming foods containing freshwater cyanobacteria, such as occurs with paralytic shellfish poisoning, has been confirmed. There are no known food vectors, such as shellfish, to concentrate toxins of freshwater cyanobacteria in the human food chain. However, the decreasing water quality and increasing eutrophication of freshwater supplies mean that large growths or waterblooms of cyanobacteria are becoming more common (Paerl, 1988), increasing the probability that humans could be exposed to a toxic dose of these algae (Charmichael, 1992). Inadvertent poisoning by the freshwater blue-green algal toxin microcystin (a functional homolog of okadaic acid) in kidney dialysis machines in Mexico has been confirmed as the cause of 30 deaths. Incomplete municipal water treatment was identified as the culprit. Other Human Routes of Exposure In the preceding section, the concern has been on the accumulation of natural toxins in seafood. This concern is well-founded, for the adulterated seafood can

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Page 67 have worldwide distribution as a result of international food marketing practices. But, in localized areas where the blooms occur, a variety of physical perturbations can result in the ejection of active toxin into the air as aerosols. The agents are neither noxious gases nor are they vapors. Rather, the toxins become associated with micro-particles of water resulting from the bursting of bubbles at the water surface. Depending upon the length of time in the airborne state, water can evaporate from the aerosol particles leaving dry salt with toxin coating the particle or entrapped within it. Only two types of toxic blooms are known to affect people by inhalation: Gynmodinium breve (Florida red tide) and Pfiesteria. The classic example of noxious natural toxins being liberated in aerosolized form is the Florida red tide and its brevetoxins. This phenomenon has been described for over 100 years. During Florida red tide, persons on the beaches experience a tightness of breath, mucous discharge from the nose, coughing and sneezing, and tearing eyes and a burning sensation in mucous membranes. Airborne toxin can travel far inland, and removal of persons to a toxin-free environment or the donning of a particle filtration face mask relieves the debilitating symptoms. It is the same toxins, or brevetoxins, that cause this effect as cause the NSP described earlier. These toxins cause their noxious effects at concentrations in air in the femto- to pico-gram per liter range. Pfiesteria piscicida (Burkholder et al., 1993), Cryptoperidinopsis brodyii nov. gen. nov. sp. (Steidinger, Landsberg, and Truby, In Review) and several other Pfiesteria-like heterotrophic dinoflagellates have been linked to lesioned fish kills in eastern United States coastal waters (Burkholder et al., 1993). Characteristically these events occur in brackish water (<15 ppt salinity) during the warmest part of the year in slow moving waters with lower oxygen content. While reports suggest that exposure to estuarine waters in Maryland during fish kills in the late summer and fall 1997 caused neurocognitive deficits in several individuals, the Centers for Disease Control and Prevention is using the term "estuary associated syndrome" to describe the phenomenon associated with such exposure. This is based on a review of the Maryland findings and the inability to attribute the adverse effects to a specific dinoflagellate or toxin (Smith and Music, 1998). However, another recent report correlated the level of exposure to waters containing Pfiesteria or Pfiesteria-like dinoflagellates with the likelihood of developing learning and memory difficulties (Grattan et al., 1998). A number of different genera may be involved and several may produce toxins. Unpublished reports of two P. piscicida toxins suggest that one is a water-soluble neurologic agent and another is a lipid-soluble dermonecrotic agent. The present difficulty in the identification and characterization of these toxins might be explained if these particular toxins degrade comparatively rapidly in the environment. There is no evidence to date of food chain contamination from P. piscicida or Pfiesteria-like heterotrophs, unlike the other heat- and cold-stable dinoflagellate toxins known to cause human illness primarily via consumption of contaminated shellfish

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Page 68 or finfish. Pfiesteria and Pfiesteria-like species are the subject of intensive investigation by researchers from Maryland to Florida of the potential causal links between the presence of these heterotrophic dinoflagellates and fish kills, fish lesions, and human health (Buck et al., 1997). The recent identification of a fungus in menhaden fish lesions, Aphanomyces, by a team at the U.S. Geological Survey (USGS) implicates it in lesioned fish episodes and makes the Pfiesteria story much more complicated. The USGS team found the fungus in 95 percent of lesions on fish taken from the Chesapeake Bay in 1997 during an outbreak of Pfiesteria (Vicky Blazer, fish pathologist at the USGS, personal communication). Research Requirements Aimed at Diagnostics, Therapeutics, and Prevention The ecology of each harmful algal bloom organism is different. Many are photoauxotrophs, that is, they are photosynthetic and carry out their lives by fixing carbon and utilizing only small amounts of simple nutrients, including nitrogen and phosphorus, and essential vitamins and minerals. Some are capable of limited heterotrophy, utilizing more complete carbon compounds or consuming other organisms like bacteria. Yet others, like Pfiesteria, Cyptoperidiniopsis, Amyloodinium, and the rest of the truly heterotrophic dinoflagellates lead a predatory or parasitic existence. The mechanisms by which each organism engulf or acquires its nutrition requires further study. The factors that lead to initiation of a bloom, maintenance of the bloom, and termination of the bloom are not completely understood for any species. Plate IX shows the occurrence of HAB-related events in the United States before and after 1972. This figure illustrates the increase in the range of HABs, but the frequency of events also appears to be higher. The reasons for this expansion are unknown, but possible explanations include natural mechanisms of species dispersal and human-related phenomena such as nutrient enrichment, climatic shifts, and more accurate reporting of HAB events. As shown on the map in Plate IX, virtually all coastal regions of the United States are now subject to a variety of HAB events. Closer monitoring of the location and frequency of blooms, as well as the physical, biological, and chemical characteristics of the affected bodies of water (as called for in ECOHAB, Box 3-1) will help to resolve why HAB events are increasing in frequency and range. In addition, this monitoring will allow earlier notification of public health authorities so that they can act to reduce exposure of the public to algal toxins. The detailed mechanism of toxicity is known for only one of the HABs, saxitoxin, and in fact there is still active debate about the microscopic site of interaction of saxitoxin with nerve membranes. It is known that saxitoxin and tetrodotoxin are nearly identical in their effects, that brevetoxins and ciguatoxin are very similar, and that the microcystins and okadaic acid behave in a similar

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