Paralytic Shellfish Poisoning - Alaska Sea Grantseagrant.uaf.edu/features/PSP/PSP.pdf · 2...
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1 Marine Resources ’ ’ Marine Resources MARINE ADVISORY PROGRAM UNIVERSITY OF ALASKA In this issue: Alexandrium, the Dinoflagellate that Produces Shellfish Poisoning Toxins 8 How Toxic Are Alaska's Most Common Shellfish 10 PSP: The Bacterial Connection 12 Truths and Myths about PSP 14 Epidemiology of Paralytic Shellfish Poisoning Outbreaks in Alaska 16 Paralytic Shellfish Poisoning in the North Pacific 18 October 1996, Volume 8, Number 2 Paralytic Shellfish Poisoning: The Alaska Problem Raymond RaLonde, Marine Advisory Program, Aquaculture Specialist Imagine yourself, a few friends, and family at the beach. The weather is amazingly cooperative this time of year for Southeast Alaska, and you feel blessed to enjoy the sunshine. Even though the wind cools the temperature, the beauty of the Alaska landscape is cause enough for celebration. What a day this is! The ocean and the scenery are magnificent. A seafood feast planned for mid-afternoon has members of your party busy harvesting shellfish from the rocky beach. In less time than expected, buckets of harvested shellfish arrive at the feet of the chef. A steamer pot of boiling salt water quickly cooks the bounty, and a few minutes later the harvest is devoured with gusto. What qualities could better represent a day in the Great Land? Reluctant to disrupt the excitement of the outing, George tells you that he feels a strange tingling on his lips and face. Your spouse is also experiencing the same strange numbness on her face. You, too busy to eat much, don’t understand as each guest complains of this strange ailment. Your spouse stumbles as she carries more food to the table. George becomes dizzy and nauseous. While helping him to a beach chair, you notice the volleyball team is leaving the playing area as each person becomes listless. The game is over, and unfortunately, so is the party. What is happening to these people? Could seafood fresh from the ocean cause such a serious condition? The problem is paralytic shellfish poisoning (PSP), and there is little you can do at this point except to get these victims to a medical facility and fast. A potentially lethal event, PSP is a crisis no one wants to experience. As many coastal residents know, eating personally harvested shellfish is risky. As Alaskans you need to know about PSP, what health dangers it presents, and how you can reduce your risk of contracting this dreaded ailment. The Toxins In Alaska microscopic single-celled dinoflagellate algae of the genus Alexandrium produce PSP toxins as a normal by-product. Bivalve shellfish (two shelled shellfish, like clams and mussels) feeding on these toxic algae may accumulate PSP toxins to concentrations unsafe for human consumption. The singular term toxin is not an accurate term for PSP since there are at lease 21 molecular forms of PSP toxins. Collectively, these PSP toxins are termed saxitoxins, deriving the name from the butter clam, Saxidomus giganteus, where saxitoxins were originally extracted and identified. All the saxitoxins are neurotoxins that act to block movement of sodium through
Transcript of Paralytic Shellfish Poisoning - Alaska Sea Grantseagrant.uaf.edu/features/PSP/PSP.pdf · 2...
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Marine Resources’’
Marine ResourcesMARINE ADVISORY PROGRAMUNIVERSITY OF ALASKA
In this issue:
Alexandrium, the Dinoflagellatethat Produces ShellfishPoisoning Toxins 8
How Toxic Are Alaska's MostCommon Shellfish 10
PSP: The BacterialConnection 12
Truths and Myths about PSP 14
Epidemiology of ParalyticShellfish Poisoning Outbreaksin Alaska 16
Paralytic Shellfish Poisoningin the North Pacific 18
October 1996, Volume 8, Number 2
Paralytic Shellfish Poisoning: The Alaska ProblemRaymond RaLonde, Marine Advisory Program, Aquaculture Specialist
Imagine yourself, a few friends, and family at the beach. The weather isamazingly cooperative this time of year for Southeast Alaska, and you feelblessed to enjoy the sunshine. Even though the wind cools the temperature,the beauty of the Alaska landscape is cause enough for celebration. What aday this is! The ocean and the scenery are magnificent.
A seafood feast planned for mid-afternoon has members of your party busyharvesting shellfish from the rocky beach. In less time than expected, bucketsof harvested shellfish arrive at the feet of the chef. A steamer pot of boilingsalt water quickly cooks the bounty, and a few minutes later the harvest isdevoured with gusto. What qualities could better represent a day in theGreat Land?
Reluctant to disrupt the excitement of the outing, George tells you that hefeels a strange tingling on his lips and face. Your spouse is also experiencingthe same strange numbness on her face. You, too busy to eat much, don’tunderstand as each guest complains of this strange ailment. Your spousestumbles as she carries more food to the table. George becomes dizzy andnauseous. While helping him to a beach chair, you notice the volleyball teamis leaving the playing area as each person becomes listless. The game is over,and unfortunately, so is the party.
What is happening to these people? Could seafood fresh from the oceancause such a serious condition?
The problem is paralytic shellfish poisoning (PSP), and there is little you cando at this point except to get these victims to a medical facility and fast. Apotentially lethal event, PSP is a crisis no one wants to experience. As manycoastal residents know, eating personally harvested shellfish is risky. AsAlaskans you need to know about PSP, what health dangers it presents, andhow you can reduce your risk of contracting this dreaded ailment.
The ToxinsIn Alaska microscopic single-celled dinoflagellate algae of the genusAlexandrium produce PSP toxins as a normal by-product. Bivalve shellfish(two shelled shellfish, like clams and mussels) feeding on these toxic algaemay accumulate PSP toxins to concentrations unsafe for human consumption.
The singular term toxin is not an accurate term for PSP since there are atlease 21 molecular forms of PSP toxins. Collectively, these PSP toxins aretermed saxitoxins, deriving the name from the butter clam, Saxidomusgiganteus, where saxitoxins were originally extracted and identified. All thesaxitoxins are neurotoxins that act to block movement of sodium through
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Cin shellfish
GTX3in shellfish
Figure 1: Molecular transformations change the toxicity of the saxitoxin molecule. The diagram illustrates two commontypes of chemical transformations that occur when the saxitoxin is passed on from algae to shellfish.
Epimerization
Acid Hydrolysis
Six-fold increase in toxicity
nerve cell membranes, stopping the flow ofnerve impulses causing the symptoms of PSPwhich include numbness, paralysis, and disori-entation (Mosher et al. 1964). The toxicity ofPSP toxins is estimated to be 1,000 times greaterthan cyanide and symptoms appear soon afterconsuming toxic shellfish. There is no antidotefor PSP, and all cases require immediate medicalattention that may include application of lifesupport equipment to save a victim’s life. If thedosage is low and proper medical treatment isadministered, symptoms should diminish inapproximately nine hours (Kao 1993).
Saxitoxin molecules undergo chemical transfor-mations that change one molecular form toanother. Transformations are performed by thedinoflagellate cell and by many animals thatacquire saxitoxins. One common transformation,termed epimerization, occurs when a portion ofthe original saxitoxin molecule rearranges.Scallop and mussel, for example, can performepimerization of saxitoxin they receive from thetoxic algae when the H and OSO
3- switch
locations on the number 11 position of thesaxitoxin molecule (Figure 1) (Oshima et al.1990). Such a transformation can decrease thetoxicity of the original saxitoxin by 11 times.Some transformations increase toxicity. Forexample, a six-fold increase in toxicity occurswhen a process termed acid hydrolysis separatesthe SO
3- group from position 21 on the saxitoxin
molecule (Figure 1) (Hall et al. 1990). Recall thatyour stomach is acidic and acid hydrolysis canoccur after you eat the shellfish. Numerous
other types of transformations occur as well aseventual detoxification that can render theshellfish safe for consumption.
The number of saxitoxin forms and theirtendency for spontaneous transformation aremajor factors hindering development of a simplefield test kit for measuring PSP toxins (Sullivanand Wekell 1988). Currently, only the mousebioassay test is approved by Food and DrugAdministration (FDA) because it simultaneouslymeasures the total of all the saxitoxin toxicitiesfrom a sample of shellfish tissue. Simply stated,the mouse bioassay measures the saxitoxin levelby timing the death of an 18-20 gram mousefollowing injection of fluid extracted fromshellfish tissue. Because the mouse bioassay is soreliable, PSP is less of a human health problemthan many other types of food born illnesses.
The AlgaePSP episodes in Alaska tend to be seasonal,occurring most often during late spring andsummer. Off-season occurrences of PSP aremost likely caused by retention of toxins fromthe summer. Shellfish become toxic whenenvironmental conditions enable toxic di-noflagellate cells to rapidly reproduce causinga toxic bloom.
A bloom begins as a small population of toxicdinoflagellate cells in the lag phase or in theform of resting cysts residing in the bottomsediment (Hall 1982). Environmental conditionssuch as changes in salinity, warming water
HOSO3-
3
H
HN21
O20
O18
H
NR1
13 +
1
23N
4
5
6NHH
19
NH
1011
12
OHOH14
OSO
15
NH16
2+
SO3-
17
-H
H N2
HN21
O20
O18
H
NH
13 +
1
23N
4
5
6NHH
19
NH
1011
12
OHOH14
OSO
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NH16
2+
SO3- 17
-3
H
H N2
HN21
O20
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NH
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1
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4
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6NHH
19
NH
1011
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OHOH14
15
NH16
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SO3- 17
H N2
Eleven fold decrease in toxicity
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temperature, and increased nutrients andsunlight trigger cyst germination to a vegetativestage that enables rapid reproduction. Once thedinoflagellate bloom begins, an exponentialgrowth phase causes a tremendous increase intheir population. In time, depletion of nutrientsand carbon dioxide in the water and degradedenvironmental conditions caused by the bloomdecrease population growth. A stationary phaseensures leveling off the population. At this highlevel of the bloom, the water may assume afluorescent reddish color referred to as a redtide. Continued environmental degradationincreases cell death and ultimately leads to apopulation crash. At this phase of the bloommany dinoflagellate species form resting cyststhat settle to the bottom, ready for the nextbloom. Within this bloom cycle, the most toxiccells occur generally during the middle of theexponential growth phase, while older cellstend to undergo more toxin transformations(Anderson 1990).
PSP toxicity can exhibit a geographic pattern.For example, on the Northeast Coast of theUnited States dinoflagellates are more toxic inthe more northern latitudes (Anderson 1990). InAlaska, varying toxin forms are found at differ-ent locations, but no clear pattern of toxicity hasbeen determined (Hall 1982).
Toxic dinoflagellates produce more saxitoxinwhen nitrogen is abundant. Where phosphorusis deficient, individual algal cells become moretoxic probably because the cells continuesaxitoxin production but reduced cell reproduc-tion prevents transfer of toxins to newly pro-duced cells (Anderson et al. 1990). The neteffect is that these non-reproducing cellscontinue to accumulate toxin.
Under laboratory culture, individual dinoflagel-late cells tend to have a higher toxin concentra-tions when grown at lower temperatures(Anderson 1990). Again, like phosphoruslimitation, the higher concentration may becaused by toxin production continuing duringlow temperature conditions while low tempera-tures reduce the rate of cell reproduction. Thecombined effect is higher toxin concentration incells grown at a lower temperature.
What about a beach that has toxic shellfishwhile an adjacent beach has shellfish that aretoxin free? This uneven toxicity is most likelycaused by a patchy distribution of the toxicalgae. In the ocean, cells of toxic algae aremoved, concentrated, or dispersed by winds,tides, and water currents. For example, if windsand ocean currents flow in the same direction;
their combined effect tends to concentratedrifting toxic algae. Opposing wind and currentsoften disperse the algae, decreasing the densityof toxic cells. Shellfish feeding on the moreconcentrated patches of toxic algae will likelybecome more toxic (White et al. 1993).
The ShellfishIn Alaska’s productive coastal waters, bivalveshellfish feed on a literal smorgasbord of micro-scopic algae. Bivalves are ideal conveyers of PSPtoxin because they are relatively indiscriminatefilter feeders, consume massive amounts ofalgae, are not generally killed by saxitoxins, andpass the accumulated saxitoxins on to anyanimal that eats them.
Six factors determine the concentration ofsaxitoxins in shellfish:• The amount of toxic algae in the water as
determined by the bloom size and patchiness.• The toxin content of the individual dinoflagel-late cell.• The feeding rate of the shellfish.• Avoidance of toxic algae by the shellfish.• Transformation of the consumed saxitoxin by
the shellfish into more or less toxic forms.• Selective retention and excretion of the
various forms of saxitoxins by the shellfish.
Shellfish nerve cells are not entirely immunefrom the effects of saxitoxins and degree oftolerance influences the shellfish’s ability to feedand accumulate toxins. In Alaska, the bluemussel, Mytilus edulis, can accumulate in excessof 20,000 micrograms (mg) of saxitoxin per 100grams of tissue, an extremely dangerous levelconsidering that allowable limit enforced by theFDA is 80 micrograms per 100 grams of tissue.In the Kodiak area during the summer of 1993,one death and several illnesses were attributedto blue mussels containing 19,600 mg of sax-itoxin. A concentration of saxitoxin that high willdeliver a lethal dose of 480 mg saxitoxin byconsumption of only 2.5 grams of mussel tissueor a single small mussel.
The extreme toxicity of blue mussels is dueprimarily to their relatively insensitivity to hightoxin accumulations that enables them tocontinue feeding. Their high tolerance tosaxitoxins and continued feeding on toxic algaecan result in initially toxin-free blue musselsexceeding the FDA 80 microgram saxitoxin levelin less than a 1 hour (Bricelj et al. 1990). Butterclams can be highly toxic partially because theirnerve cells appear to have a special resistance toSTX saxitoxin, one of the two most potent formsof the saxitoxins (Beitler and Liston 1990,Twarog et al. 1972).
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Table 1: PSP values for selected giant scallop tissues (in µgsaxitoxin/100 grams of shellfish tissue).
Location Date Adductor Viscera Gills Gonads MantelAkhiok June 1987 35 2,298 221 301 340Izhut Bay July 1987 58 4,945 504 1,361 243Swikshak Sept. 1987 <32 2,862 - 446 41
Data from Alaska Department of Environmental Conservation.Note: All the locations in this table are in the Kodiak Island area.
In addition, the butter clam has a distinctiveability to chemically bind the highly toxic STXsaxitoxin in their siphon tissue (Beitler andListon 1990), and they can retain PSP toxins forup to two years after initial ingestion (Hall 1982).
The Alaska steamer or littleneck clam,Protothaca staminea, becomes toxic but isgenerally less toxic than the butter clam. Thelower toxicity of the littleneck clam is due partiallyto their ability to perform unique transforma-tions that change highly toxic saxitoxins to themoderately toxic forms (Sullivan et al. 1983).
The combined effect of the littleneck clam’scapability to transform saxitoxins to less toxicforms, and the ability of butter clams to concen-trate and retain highly toxic forms can result in awide difference in toxicity between these twospecies. This toxicity difference is particularlysignificant since butter and littleneck clams cancoexist on the same beach, and, to the unskilledharvester, are similar in appearance. To exem-plify the difference, one study testing for toxicityof a mixed butter/littleneck clam populationfound that littleneck clams were about 11-25%as toxic as butter clams (Kvitek and Beitler,1991). The lesson here is that if you cannotdistinguish the difference between a butter andlittleneck clam, you should take the time tolearn and return your harvested butter clamsback to the clam bed.
The Pacific oyster, Crassostrea gigas, though notnative to Alaska is an important species foraquatic farming. The Pacific oyster tends toconsume toxic algae readily during initialcontact but decreases and eventually stopsfeeding when tissue toxin levels become high(Bardouil et al. 1993).
Saxitoxin concentrations also differ amongvarious shellfish tissues. For example, in thePacific giant scallop, Patinopectin caurinus, theadductor muscle seldom accumulates saxitoxinsabove the FDA limit, but other tissues regularlyhave high levels (Table 1). It is these highsaxitoxin concentrations in other tissues that
have prevented development of a highly valuedgonad/adductor muscle product.Another endeavor to diversify the line of scallopproducts through aquaculture development inthe Kodiak area was attempted on two bayscallop species; the pink scallop, Chlamysrubida; and spiny scallop, Chlamys hastata.This time the scallop were to be sold as a wholein-the-shell product. The effort ceased whenpersistent high saxitoxin concentrations, at timesexceeding 11,000 mg, were encountered. Whilemost of the PSP records for whole scallop hasbeen confined to the Kodiak area, consumersshould be cautious of eating whole scallopharvested anywhere in the state since toxinlevels can be very high and scallop retain toxinsfor an extended time.
The purple hinge rock scallop, Crassadomagigantea, is another popular scallop speciesfound attached to subtidal rocky substrate,predominantly in Southeast Alaska. Peculiar tothis scallop is its tendency to have a toxicadductor muscle (Beitler 1991). Although testingfor saxitoxins in purple hinge rock scallop hasnot been done in Alaska, data from BritishColumbia and the West Coast of the U.S.provides us a warning (Table 2).
The razor clam recreational fishery in Cook Inletbrings thousands of harvesters to the beachduring extreme low summer tides. A questionoften asked is “Are these clams safe to eat?” Theanswer to this question is, “Most likely, yes.”Data collected by the ADEC from the Cook Inletcommercial fishery has consistently shown thatPSP is not a problem in these razor clams. Otherlocations around the state, however, haverecorded saxitoxin concentrations in razor clamsthat are above the FDA regulatory limit. Relyingon a commercial fishery for PSP monitoringdoes have a major shortcoming because you, asa recreational harvester, do not have immediateaccess to the test results. Thus, you would haveno idea if a sample submitted by a commercialharvester failed the PSP test.
Saxitoxins also migrate to different tissues andmay undergo further transformation in theprocess. In the butter clam, for example, highsaxitoxin concentrations begin to accumulate inthe digestive system after initial consumption oftoxic algae. Within one month, however,saxitoxins migrate to the siphon and undergotransformation from the relatively less toxic GTXsaxitoxins to the highly toxic STX form (Beitlerand Liston 1990).
Shellfish eventually clean themselves of saxitox-ins through a process termed depuration. Thetime required for saxitoxin depuration is greatly
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Table 2: PSP toxin concentrations in the purple hingerock scallop (µg saxitoxin/100 grams of tissue).
Location Adductor Viscera Whole BodyBritish Columbia1 130 2,500 1,200Washington1 229 2,036 295California2 2,000 26,000 13,593
Data from: 1Department of Fisheries and Oceans 1989 2Sharpe 1981
influenced by environmental conditions and isextremely variable and unpredictable for wildgrown shellfish. As an example, blue musselscan reduce saxitoxins from 700 mg to below theFDA 80 mg limit within 20 days, but the processmay take over 50 days (Desbins et al. 1990). Inthe Skagway area, blue mussels required 40days to reduce saxitoxins from 1,098 mg tobelow the 80 mg FDA requirement (ADEC data).Any attempt to estimate the depuration time fora shellfish population following a PSP event isdangerous; primarily because there is no way ofknowing the size and duration of the toxicdinoflagellate bloom, and recurrent blooms canrecontaminate shellfish.
The PSP problem in not isolated to just thebivalve shellfish. In recent years the Alaska crabfishery was drastically impacted when PSP wasfound in crab viscera. Although crab viscera isconsumed in small portions, the discovery ofPSP caused a flurry of regulations meant toassure consumer safety. A major concern thatdiffers from bivalve shellfish is the fact that crabare opportunistic feeders, not filter feeders, andtoxicity may vary significantly for each crabbased upon the toxins contained in the foodthey choose to eat. Since initial concerns of PSPin crabs, regulations developed by the ADECand cooperative agreements with the commer-cial crab fishery, now assure the safety of crabviscera. Since saxitoxins are water soluble,boiling live crab with the viscera in tack mayspread the toxins from the viscera to othertissues. To prevent spreading of toxins, theADEC recommends cleaning crabs of viscerabefore boiling.
The Food WebHow does PSP effect the marine environment?The answer to that question is difficult andextensive research reveals few conclusions.
Zooplankton, microscopic animals drifting inwater, feed on toxic dinoflagellates and concen-trate the saxitoxins, but these tiny animals aregenerally more sensitive to the effects ofsaxitoxins than adult bivalve shellfish (Hwangand Chueh, 1990). Although lethal to manyzooplankton, saxitoxins can be passed along thefood chain by zooplankton that limit toxinaccumulation by reducing their feeding. Highsaxitoxin levels also impaired zooplankton;swimming ability causing them to become easyprey for fish, mammals, and birds (Buskey andStockwell, 1993). Saxitoxin containing zooplank-ton have been implicated in fish kills (White1981, Smayda 1992) and deaths of marine mam-mals after eating toxic fish (Geraci et al. 1989).
Some marine mammals and birds have adaptedto living in an environment of marine toxins.For example, sea otters can detect harmfulconcentrations of saxitoxins and avoid eatingtoxic shellfish (Kvitek et al. 1991). The glaucous-winged gull has evolved an aversion to PSP andeven young chicks regurgitate contaminatedshellfish (Kvitek 1991). Marine biotoxins play asignificant role in our marine environment andfuture efforts to measure the sublethal effects oftoxic algae on marine organisms and the conse-quences for the marine ecosystems will be anelusive endeavor.
The Alaska ProblemEpisodes of PSP in Alaska are centuries old, buton a global scale, toxic algae blooms are becom-ing an increasing menace. Attributed to man-caused nutrient enrichment of coastal waters(Anderson 1989, Smayda 1992), uncontrolledballast water discharge from internationalshipping (Jones 1991), and possibly climaticchanges, an international effort is now underway
to explore solutions to the problem. Of practicalsignificance is recognition that unpredictablechanges in the ocean environment invalidatesuse of historical information as a sole source inforecasting toxic algal blooms and provides noguarantee that shellfish, historically free of PSPtoxins, will remain in that condition.
The economic consequences of the PSP problemhas drastically impacted development of a clamfishery in Alaska where an estimated 50 millionpounds are available for harvest (U.S. Depart-ment of Interior 1968). With harvest of 5 millionpounds annually, a wholesale value of over $5million could be realized.
In Alaska, widespread indifference of recre-ational and subsistence harvesters to PSPwarnings causes considerable concern for theAlaska Division of Public Health and the AlaskaDepartment of Environmental Conservation,agencies responsible for ensuring public health.
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A recent survey of Kodiak Island conducted bythe Alaska Division of Public Health found thatthe level of risk of contracting PSP is not equallyshared among all shellfish consumers. Surveyresults found that:
• Long-term residents (at least 23 years) are 11.8times more likely to report symptoms of PSPthan short terms residents.
• Alaska Natives are 11.6 time more likely toreport symptoms of PSP than non-Natives.
• If you have eaten shellfish for longer than 20years, you are 5.4 times more likely to reportsymptoms of PSP.
• Residents of the Alaska Native village of OldHarbor are 3 times more likely to reportsymptoms of PSP than residents of Kodiak.
One of the most disturbing findings of the studyshowed that people who knew nothing aboutthe lethal potential of PSP had the same fre-quency of reporting symptoms of PSP as thosewho knew PSP could cause death (Gessner andSchloss 1996).
Non-English speaking residents may havegreater risk of exposure to PSP because thecommunication barrier hampers alerting themof PSP warnings. One of the latest victims inKodiak was a Laotian resident.
Many myths about PSP have lead to practicesalleged to improve your chances of avoidingillness. The Kodiak study found two-thirds ofthe residents that consumed shellfish fromuntested beaches believed it was possible tocollect, prepare, or test shellfish in such a waythat PSP could be prevented. Rather thanreducing the risk of PSP, these unproven prac-tices may give the consumer a false sense ofsecurity that may actually increase their risk ofa PSP incident.
PSP is a complex problem, but you can stillreduce your risk of encountering PSP. Obvi-ously, the most acceptable decision is not toconsume untested shellfish but purchase shell-fish from a seafood retailer or shellfish farm thatis required to sell only tested product. However,many people will continue to consume shellfishdespite the warnings, and willingly accept anunknown risk with each meal.
Some shellfish consumers take absurdly highrisks. For example, eating whole blue musselsfrom the Kodiak area during the summer is aninvitation for PSP. When considering harvestingshellfish the potential consumer must at aminimum consider:
• The recent history of PSP for the area.• The species harvested and their ability to
concentrate and retain toxin.• The season of the year.• The method of cleaning and preparing
the shellfish (i.e., whole scallop vs.adductor muscle).
As a harvester of wild shellfish, you cannot haveenough information to absolutely guarantee thatuntested shellfish are free of dangerous levels ofPSP toxins.
Avoid myths surrounding PSP prevention. Themere fact that in all five outbreaks in Kodiak in1993, none showed any evidence of a red tideshould be ample evidence that water color isnot a reliable indicator of PSP.
A major problem in Alaska is under-reporting ofPSP by persons experiencing minor symptoms.In some instances, if victims had reported theirPSP symptoms to a medical facility, moreserious consequences could have been averted.
It is your obligation to report even minorsymptoms of PSP to your local medical careunit. Your action may save someone’s life.
An obvious problem in Alaska is the lack ofdata on toxic algae blooms, shellfish testing, andreporting of PSP outbreaks. The Alaska Divisionof Public Health and the ADEC are very inter-ested in recruiting public assistance in PSPmonitoring. The more information we collectabout the frequency and distribution of redtides, toxic algae blooms, and PSP episodes themore likely we are to understand the environ-mental impacts of PSP and develop strategies toprevent illness.
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Kvitek, R.G., A.R. DeGange, and M.K. Beitler. 1991. Paralyticshellfish poisoning toxins mediated feeding behavior of sea otters.Limnology and Oceanography. 36(3):393-404.
Mosher, H.S., F.A. Fuhrman, H.S. Buchwald, and H.G. Fischer.1964. Tarichatoxin-Tetrodotoxin: A potent neurotoxin. Science.144:1100.
Oshima, T., K. Sugino, H. Itakura, M. Hirota, and T. Yasumoto. 1990.Comparative studies on paralytic shellfish toxin profile of dinoflagel-lates and bivalves. Pages 479-485 in E. Graneli, B. Sundstrom, L. Edler,and D.M. Anderson, editors. Toxic Marine Phytoplankton. ElsevierScience Publications.
Sharpe, C.A. 1981. Paralytic shellfish poison, California - Summer1980. State of California Department of Health Services - SanitaryEngineering Section
Smayda, T.J. 1992. Global epidemic of noxious phytoplanktonblooms in the sea: evidence for a global epidemic. Pages 275-307in K. Sherman, L.M. Alexander, and B.D. Gold, editors. Food Chains:Models and Management of Large Marine Ecosystems. Westview Press.San Francisco.
Sullivan, J. and W.T. Iwaka, and J. Liston. 1983. Enzyme transfor-mations of PSP toxins in the littleneck clams, Prototheca staminea.Biochemical and Biophysical Research Communications.114(2):465-472.
Sullivan, J. and M. Wekell. 1988. Detection of paralytic shellfishtoxins. Pages 87-106 in T. Tu. Anthony, editor. Handbook ofNatural Toxins, Volume 3. Marcel Dekker. Inc., New York.
Twarog. B.M., T. Hidaka, and H. Yamaguchi. 1972. Resistance oftetrodotoxin and saxitoxin in nerves of bivalve molluscs. Toxicon.10:273-278.
United States Department of the Interior. 1968. The potential ofAlaska’s fishery resources. Newsletter to Alaska Fishermen andProcessors. Number 9, September 13, Juneau, Alaska.
White A.W. 1981. Marine zooplankton can accumulate and retaindinoflagellate toxins and cause fish kills. Limnology and Oceanog-raphy. 26:103-109.
White, A.W., S.E. Shumway, J. Nassif, and D. Whittaker. 1993.Variation in levels of paralytic shellfish toxins among individualshellfish. Pages 441-445 in T.J. Smayda and T. Shimizu, editors.Toxic Phytoplankton Blooms in the Sea. Elsevier Science Publications.
8
Alexandrium,theDinoflagellatethatProducesShellfishPoisoningToxinsRita A. Horner,School ofOceanography,University ofWashington,Seattle,Washington
Figure 1:Alexandriumcatenella 7-celled chain
In Alaska, and elsewhere in the Pacific North-west, paralytic shellfish poisoning (PSP) iscaused by dinoflagellates in the genusAlexandrium (Figure 1). First described as aspecies in the genus Gonyaulax (Whedon andKofoid 1936), the toxin-producing species werelater transferred to Protogonyaulax (Taylor1979), and recently to Alexandrium (Balech1985, Steidinger 1990).
Much of the confusion has been resolved by acloser examination of cellular morphology ofthe toxin-producing species. In addition, theAlexandrium show much variation in morphol-ogy caused by natural variation, sexual repro-duction that increases genetic variation, thediscovery of the cyst stage that is structurallydifferent from the vegetative cell stage, andenvironmental conditions. Currently, there are22 species in this genus (Balech 1985).
The vegetative stage of Alexandrium is motileand have a theca (an outer covering or cell wall)made of cellulose plates. The arrangement ofthese plates, though there may be some variabil-ity, is a characteristic used for identification(Balech 1985). The plates are most easily seen ifthe cells are gently squashed to remove the cellcontents. The cells are divided into upper andlower parts by a central groove (girdle) with theends displaced about one girdle width. Alongitudinal groove (sulcus) runs from the girdleto the posterior end of the cell (Figure 2). Twoflagella, whip-like structures used for swimming,are present, one encircling the cell in the girdle,the other, lying along the sulcus and trailingbehind the cell. Cells are round to oval in shapeand range in size from about 20-50 mm indiameter. They may be single or occur in chains.Identification is difficult unless chains arepresent and single cells may easily be mistakenfor other small, brown-pigmented dinoflagellatesincluding Scrippsiella trochoidea.
General features of the genus include thecharacteristic shape and arrangement of surfaceplates, girdle displacement about one girdlewidth, no spines or horns, thin cell walls, acharacteristic apical pore plate, the presence orabsence of a ventral pore, and smooth-walledcysts. Species are distinguished by the size andshape of the cells, size and shape of some ofthe thecal plates, presence or absence of aventral pore, size and shape of some of thegirdle plates, and the relationship between theapical pore plate and the more-or-less diamond-shaped plate ventral to it. A key to the speciesis found in Balech (1985).
Based on analysis of small-subunit ribosomalRNA genes, three species of Alexandrium occuron the North American west coast (Scholin andAnderson 1994). A. catenella (Whedon andKofoid) Balech occurs from southern Californiato southeast Alaska, forms chains, blooms whenthe water temperature is about 20°C, and occursin both estuarine and open coast environments;it lacks a ventral pore. A. tamarense (Lebour)Balech, prefers cooler temperatures and lesssaline water than A. catenella and has a ventralpore. It has been found at Unimak Island in theGulf of Alaska. A. fundyense Balech, originallydescribed from the Bay of Fundy, is small, lacksa ventral pore, and has been found at PorpoiseIsland, Alaska. Other species identified usingstandard morphological characteristics includeA. acatenella (Whedon and Kofoid) Balech, A.ostenfeldi (Paulsen) Balech, A. hiranoi Kita andFukuyo (Taylor and Horner 1994). A. catenella,A. acatenella, and A. tamarense are part of thesame species complex, but in British Columbia,at least, they tend to have different distributions(Taylor and Horner 1994). Elsewhere in thePacific Northwest, their distribution is notwell-known.
Two kinds of cysts may occur in the life cycle,both with smooth cell walls (Figure 2). Pelliclecysts are vegetative and are produced frommotile, vegetative cells in response to environ-mental stress, including temperature changesand nutrient depletion. These cysts have limiteddurability and do not overwinter. They aresmooth-walled, deeply pigmented, and have arequired dormancy period. They are resistant toenvironmental extremes and may provide seedpopulations for future blooms if conditions forgermination are right. These resting cysts maybe transported in the same manner as sedimentparticles, including by normal water currents orcatastrophic events such as hurricanes. As aresult, they may germinate far from their placeof origin and initiate blooms in new areas. Cystformation may be a factor in the decline ofblooms. Cysts are also toxic and are thus asource of toxicity to the food chain.
9
The distribution of Alexandrium in Alaskanwaters is not well-known and historical recordsare sparse. Reasons for this include the longcoastline and the lack of samples from manysites. Moreover, much of what is known orsuspected about the distribution of toxic cellscomes from records of toxicity in shellfish, notfrom knowledge of the biology of the di-noflagellates. Alexandrium-like cells have beenfound at a number of places in southeast andsouthcentral Alaska, but the problem has beento correlate the abundance of a causativeorganism, presumably Alexandrium spp., withthe timing, levels, and geographic distribution oftoxin in the shellfish (Hall 1982). Consequently,Hall (1982) sampled the water column andsediments from Dutch Harbor to Ketchikan formotile cells or cysts and isolated about 50strains from 11 sites. In culture studies he foundthat toxin content per cell varied substantiallywithin a strain, but toxin composition of a strainchanged little with culture conditions or stage ofgrowth. However, regional patterns of toxincomposition were found where strains from oneregion had the same toxin composition, whilestrains from other regions had different compo-sitions. Shellfish toxicity should vary in a similarmanner according to Hall (1982).
Thus, it is apparent that there are no easyanswers to the problem of shellfish toxicity andcausative species in Alaska. Without compre-hensive phytoplankton and/or shellfish monitor-ing programs, there is currently no way to ensurethat shellfish are safe for human consumption.
ReferencesAnderson, D.M. and D. Wall. 1978. Potential importance ofbenthic cysts of Gonyaulax tamarensis and G. excavata ininitiating toxic dinoflagellate blooms. Journal of Phycology.14:224-234.
Balech, E. 1985. The genus Alexandrium or Gonyaulax ofthe tamarensis group. Pages 33-38, in D.M. Anderson, A.W.White, and D.G. Baden, editors. Toxic dinoflagellates.Elsevier, New York.
Hall, S. 1982. Toxins and toxicity of Protogonyaulax fromthe northeast Pacific. Ph.D. Thesis, University of Alaska,Fairbanks. 196 pp.
Scholin, C. A. and D.M. Anderson. 1994. Identification ofgroup and strain-specific genetic markers for globallydistributed Alexandrium (Dinophyceae). I. RFLP analysis ofSSU rRNA genes. Journal of Phycology 30:744-745.
Streidinger, K.A. 1990. Species of the tamarensis/catanellagroup of Gonyaulax and the fucoxanthin derivative-containing Gymnodinioids. Pages 11-16, in E. Graneli, B.Sundstrom, L. Edler, and D.M. Anderson, editors. Toxicdinoflagellate blooms. Elsevier, North Holland, New York.
Taylor, F.J.R. and R.A. Horner. 1994. Red tides and otherproblems with harmful algal bloom in Pacific Northwestcoastal waters. Pages 175-186, in R.C.H. Wilson, R.J.Beamish, F. Aitkens, and J. Bell, editors. Review of themarine environment and biota of Strait of Georgia, PugetSound and Juan de Fuca Strait: Proceedings of the BC/Washington Symposium on the Marine Environment, Jan 13& 14, 1994. Can. Tech. Rep. Fish. Aquat Sci. 1948.
Whedon, W.F. and C.A. Kofoid. 1936. Dinoflagellata of theSan Francisco region. I. On the skeletal morphology of twonew species, Gonyaulax cantenella and G. acatenella,University of California Publication. Zoology 41(4):25-34.
Figure 2: Generalized life cycle of Alexandrium.Figure h shows characteristic thecal plates for A.catenella; 1 is the ventral view, 2 is the apicalpore plate, the thecal plate closest to the portplate, and a sulcal plate. Figures a-g, and imodified from D.M. Anderson; Figure hmodified from Balech (1985).
AlexandriumLife Cycle Vegetative Cell Division
New MotileCell
YoungGermling
Hypnocyst
Planozygote
Gamete Fusion
Gametes
Pellicle cyst
Sulcus
Girdle
Thecaplate
ab
c
d
ef
g
h
i 12
10
Pacific Razor ClamSiliqua patulaDistribution: Alaska to mid CaliforniaHabitat: Intertidal zone, open coastsin sandSize: up to 8"Identification: Long narrow shell,thin and brittle, olive green tobrown colorToxicity: 3,294 µg toxin
Butter ClamSaxidomus giganteusDistribution: Aleutian Islands tomid CaliforniaHabitat: Intertidal zone to 120 feetdepth, on protected gravel, sandybeachesSize: up to 5"Identification: Dense shell, externalsurface with concentric rings, promi-nent growth ringsToxicity: 7,750 µg toxin
Pacific Littleneck ClamProtothaca stamineaDistribution: Aleutian Islands tomid CaliforniaHabitat: Midtidal to subtidal zone,mud to coarse gravel beachesSize: Up to 2 1/2"Identification: External surface of shellwith radiating and concentric groovesToxicity: 580 µg toxin
Softshell ClamMya arenariaDistribution: World-wide north of
mid CaliforniaHabitat: Upper tidal level mud flatsSize: Up to 6"Identification: Shell soft, easilybroken, one end of shellrounded, other end pointed,concentric rings onlyToxicity: 47 µg toxin
CockleClinocardium nuttalliDistribution: Bering Sea toSouthern CaliforniaHabitat: Interidal zone to 90feet, mud to sand beachesSize: Up to 6"Identification: Thick cupped shells,up to 35 strong ribs spreading fromthe hinge to shell marginToxicity: 2,252 µg toxin
GeoduckPanopea abruptaDistribution: Sitka, Alaska toGulf of CaliforniaHabitat: Intertidal to deep water,buried deeply in sand and mud bottomSize: Shell up to 8"Identification: Shells heavy, oneend of shell rounded the other endflat, rough concentric grooves onshell surface.Toxicity of viscera: 1,526 µg toxin
Blue MusselMytilus edulisDistribution: Northern HemisphereHabitat: Rocky intertidal areas ofexposed and protected coastlineSize: Up to 4"Identification: Blue/black to brown-ish shell, shell pointed at one end andround at the other, has a threadlikestructure to attach to substrateToxicity: 20,000 µg toxin
Toxicity levels shown are the highest recorded in Alaska. The FDA
How Toxic Are Alaska's
Concentric
rings
Radiating
grooves
or rib
Shellfish drawings from “Intertidal Bivalves: AGuide to Common Marine Bivalves of Alaska”,Nora R. Foster. 1991. University of Alaska Press
11
Spiny ScallopChlamys hastataDistribution: Gulf of Alaskato CaliforniaHabitat: Low intertidal area to400 feet depthSize: Up to 3 1/2"Identification: Shell thin andflattened, auricles uneven size, 20-30ribs on each shell, ribs spiny texturedToxicity: 11,945 µg toxin (whole)
Horse (Gaper) ClamTresus capaxDistribution: Shumagin Islands,Alaska to CaliforniaHabitat: Intertidal zoneimbedded deeplySize: Up to 8"Identification: Shell large and thick,wide gape between shells at posteriorend when held together, dark
covering (periostracum) on shellsurface often partially worn offToxicity: 281 µg toxin
Alaska Razor ClamSiliqua altaDistribution: Bering Sea to CookInletHabitat: Intertidal zone to 30 feet onopen sandy beachesSize: Up to 6"Identification: Long narrow shapedshell, shell thin and brittle, brown toolive green colorToxicity: 3,294 µg toxin
Purple Hinge Rock ScallopCrassadoma giganteaDistribution: Aleutian Islands toSouthern CaliforniaHabitat: Low tidal area to 200feet depth, attached to rocks andin crevices.Size: Up to 10"Identification: Very heavy roughshell, purple color hinge area whenshell openToxicity: 2,000 µg toxin (whole)
Pink ScallopChlamys rubidaDistribution: Bering Sea tomid CaliforniaHabitat: Low tidal area to 900 feetdepth, rocky shorelineSize: Up to 2 1/2"Identification: Shell thin andflattened, 20-30 ribs on each shell,auricles uneven size, red/pink on oneshell, opposite shell, color paleToxicity: 11,945 µg toxin (whole)
Pacific OysterCrassostrea gigasDistribution: Kachemak Bayto CaliforniaHabitat: Intertidal in mud to rockybeaches. In Alaska only on aquaticfarms, but may be a few smallpopulations in southern southeasternAlaska. Does not reproduce inAlaska watersSize: Up to 8"Identification: Shell irregular shape,rough surface, upper shell cuppedwhile lower shell flatToxicity: 910 µg toxin
considers anything above 80 µg (micrograms) of toxin not safe to consume.
Most Common Shellfish ?
12
Paralytic shellfish poisoning (PSP) is a persistentproblem in Alaska and along the West Coast ofthe United States. PSP is caused by a neurologi-cally damaging saxitoxin that is assumed to beproduced by a planktonic dinoflagellate,Alexandrium cantenella (Read: Alexandrium,the Dinoflagellate that Produces ShellfishPoisoning Toxins). This may very well be true,but recent data questions this assumption andsurfaces suspicions that bacteria, not dinoflagel-lates, produce saxitoxins.
Questions about the role of dinoflagellates inAlaska producing saxitoxins began in the mid-1960s when a study by the University of Alaskain southeastern Alaska failed to find a relation-ship between the abundance of A. cantenella inthe water and the occurrence of PSP (Chang1971). Other studies found a correlation be-tween the presences of A. cantenella and PSP,however, the very small number of A.cantenella collected in the water samples couldnot account for the high level of toxin (Sparks1966, Neal 1967). In 1973, the first direct linkbetween A. cantenella and PSP was recorded bySimmerman and McMahon (1976) when severalfamilies ate butter clams collected near the boatharbor in Tenakee. The case was proven whentwo unsuspecting victims developed PSP fromeating clams harvested from a beach whereasothers, having recently eaten clams from thesame beach, had no toxic reaction. An analysisof the uneaten portions of clams, which in-cluded the gills and digestive gland, showedhigh levels of saxitoxin. Saxitoxin in theseparticular tissues indicated that the toxic condi-tions were recent since toxin in butter clamsmoves into the siphon after a period of time.Fortuitously, only five days before the toxinproblem, the Alaska Department of Environmen-tal Conservation RV Maybeso had been in thearea and had observed unusual bioluminescencein Tenakee Harbor prompting the scientists tocollect water samples. Later examination of thesamples found high numbers of A. cantenella.Later, Hall (1982) confirmed the “dinoflagellateconnection” when he induced resting cysts of A.cantenella to germinate and then subsequentlyproduced saxitoxin.
During the same time period the PSP story wasalso unfolding in laboratories around the world.The general scenario emerging was similar toAlaska, in some locations and at certain timesthere were inconsistencies between toxinproduction and algae abundance, whereas inother locations there was consistent agreement.Adding to the confusion were findings thatsome geographical strains of dinoflagellatesproduce more toxin while others produced littleor no toxin. Silva and Sousa (1981) made a
remarkable discovery when they transformed anon-toxic dinoflagellate strain to a toxin pro-ducer by simply inoculating the non-toxic strainwith a bacterium, Pseudomonas sp., isolatedfrom a toxin-producing dinoflagellate. Thisobservation, though exciting, could not confirmwhich organism, the bacterium or the di-noflagellate, produced the toxin. Nonetheless,this observation, linked with the fact thatdinoflagellates routinely harbor intra cellularbacteria (Bold and Wynn, 1979), prompted thequestion “are bacteria the real source of saxitox-ins?” Since most scientists studying saxitoxinswere phycologists (algae specialists), theyemphatically responded: “no way!”
The implication that bacteria produce thesaxitoxins has met with some resistance fromphycologists. This resistance is due in part tothe complex associations that occur betweenalgae and bacteria, but there is clear implicationthat phycologists could say with a clear con-science: “bacteria are not producing saxitoxins,they are only inducing the alga to synthesizethe toxins.”
Most phycologists accepted the idea thatbacteria may have a direct role in saxitoxinproduction by inducing the algae to producetoxin rather than directly producing saxitoxin.Many investigators started examining their algalcultures more closely and using the electronmicroscope to look for bacteria within thedinoflagellate cell. Kodama and colleagues,attempting to prove the hypothesis that bacteriacan produce saxitoxin took a more risky ap-proach (Kodama et al. 1988, 1990) by isolatingbacteria from cultured dinoflagellates and evenremoving bacteria individually from inside thedinoflagellate cells. They found that undercertain precise growing conditions bacteriumcould indeed synthesize saxitoxins. This findingwas a shock to everyone, especially the phy-cologist, many of whom had spent a lot of timeconfirming that bacteria were NOT present intheir toxic dinoflagellate cultures.
The race was on. Who makes saxitoxins? CouldKodama’s work be repeated? For more than fiveyears several labs attempted to culture saxitoxinproducing bacteria, some labs even usedKodama’s original strain, but without success.Was the toxin producing bacteria an artifact or ahoax? Could the toxin detected in the originalexperiment have been a residual amountaccumulated and retained by the bacteria fromtoxin producing dinoflagellates?
Then, to everyone’s surprise, a second labdemonstrated bacterial production of toxin(Doucette and Trick 1995, Doucette 1995). The
PSP: TheBacterialConnectionF.G. Plumley,AssociateProfessor, UAFInstitute of MarineScience,and Z. Wei, Ph.D.graduate student
13
BotulinusToxin A
Strychnine Muscarin SodiumCyanide
DiptheriaToxin
CobraNeurotoxin
ParalyticShellfishPoison orSaxitoxin
TetanusToxin
1100
500
90.30.3.0001.00003
(mushroom)
10000
How Much Will Kill Me?
Micrograms per kilograms per body weight.
leas
t dea
dly
dead
ly
amount of toxin was very small, but the experi-mental methodology was performed withextreme care and the results were conclusive.This time the results were more acceptable tophycologists because more recent studies alsoshowed that freshwater cyanobacteria (formerlyknown as blue-green algae) also producedsaxitoxins (reviewed in Carmichael et al. 1990;Carmichael and Falconer 1993). The importanceof this event is apparent in that the saxitoxinproducing cyanobacteria are more closelyaligned taxonomically to bacteria than algae.The fact that this process occurs in freshwaterrather than marine systems was then, and still is,a matter of concern.
There remains, however, several unansweredquestions. First, are dinoflagellates able tosynthesize saxitoxins in the absence of bacteria?Second, if bacteria contained within the di-noflagellate cell are responsible for saxitoxinsynthesis, how in nature, can they produce thelarge amount detected when in laboratoryculture only minute quantities are produced?Third, if both the bacteria and the dinoflagellatehave necessary roles in toxin production, howdid such an evolutionarily separated pair oforganisms develop such a capability?
The answers to the first two questions are nowbeing investigated by a number of laboratoriesaround the world. For the first problem, labora-tories are again checking their toxin producingdinoflagellate cultures for bacteria.
A problem with this type of investigation is thattheoretically you cannot prove that somethingdoes not exist, you can only demonstrate thatyou have been unable to find it. By the samelogic, the absence of data cannot be taken as anabsence of the event. Bacteria may indeed be ina dinoflagellate culture, but scientists have notbeen able to find them or detect their influenceon toxin production. For the second question,several labs are growing bacteria under a varietyof conditions to determine if saxitoxin produc-tion can be increased.
The answer to the third question is the area ofresearch being conducted in the labora-tory of these authors. We areattempting to clone one ormore genes that encode theenzymes required to makesaxitoxins. Once this task iscompleted, the cloned DNAfragments can then be used as“probes” to determine who elseproduces saxitoxins. To dateour results have been less thanencouraging, primarily because
the bacteria that produce saxitoxin are difficultto analyze at the molecular level.
One hypothesis we are pursuing is that the toxinproducing genes evolved only once, originatingin the bacteria, then later were transferred todinoflagellates by a recently discovered processcalled trans-kingdom sex (Amabile-Cuevas andChicurel 1993). That bacteria may be able totransfer genetic information across kingdomboundaries from bacteria to algae cells. This hasprofound evolutionary implications for severalcontroversial issues in biology, possibly includ-ing a better understanding of the PSP problem.
References
Amabile-Cuevas, C.F. and M.E. Chicurel. 1993. Horizontalgene transfer. American Scientist. 81:332-341.
Bold, J.C. and M.J. Wynn. 1978. Introduction to theAlgae: Structure and Reproduction. Prentice Hall, Inc.,N.J. 706 pp.
Carmichael, W.W., N.A. Mahmood, and E.G. Hyde, 1990.Natural toxins from cyanobacteria (blue-green algae).Pages 87-106, in S. Hall and G. Strichartz, editors. MarineToxins: Origins, Structure and Molecular Pharmacology.American Chemical Society, Washington, D.C.
Carmichael, W.W. and I.R. Falconer. 1993. Diseasesrelated to freshwater blue-green algal toxins and controlmeasures. Pages 187-209, in I.R. Falconer, editor. AlgalToxins in Seafood and Drinking Water. Academic PressLimited.
Chang, J.C. 1971. An ecological study of butter-clam(Saxidomus giganteus) toxicity in Southeast Alaska. M.S.Thesis, University of Alaska Fairbanks, Alaska. 94 pp.
references continued on page 15
14
Are months with an “r” are safe for eatingshellfish?
No. Months without an “r” occur during thesummer when toxic dinoflagellate blooms thatcause PSP most often occur. With the unlikelypossibility that shellfish will become toxicoutside the summer season, consumers assumeshellfish are safe to eat. This answer is wrong inthree ways.
1. In some locations in Alaska shellfish remainhighly toxic in the spring and fall. PSP outbreakshave occurred in all seasons.
2. Toxic dinoflagellate algae can form cyststhat reside in the sediment during the non-bloom seasons. These cysts are as toxic as thesuspended vegetative form that are presentduring a toxic bloom. Shellfish, being bottomdwelling filter feeders, can continue to consumecysts during non-bloom periods and accumulatePSP toxin.
3. Some shellfish can retain the PSP toxin for along period. Blue mussels in the Skagway areatook 28 days before they were safe to eat. Sucha long retention time could extend into the fallseason. Other shellfish like the butter clams canchemically bind PSP toxin and retain it for aslong as two years.
Is there an antidote for PSP?
No. PSP is a neurotoxin that blocks movementof sodium through membranes of nerve cells.Without sodium transmission, nerve cells cannotfunction. This leads ultimately to the symptomsof PSP: numbness, paralysis, respiratory failure,and coma. There is no specific antidote to stopthe effect of PSP toxicity.
Is there a treatment for PSP?
Yes. Induce vomiting by sticking a finger downthe throat, drinking warm saltwater, or takingSyrup of Ipecac to expel shellfish from thevictim’s stomach. Treat the victim for shock andtransport to a medical facility. Application of lifesupport services at the medical care facility maybe necessary to sustain the life of the victim.Reduction of symptoms normally occurs within9 hours and complete recovery usually within 24hours. You must not underestimate the serious-ness of PSP. Once the symptoms begin toappear, the victim must be transported immedi-ately to a medical care facility.
Is a toxic algae bloom the same thing as ared tide?
Not always. A number of marine organisms inAlaska cause red tides, including non-toxicdinoflagellates of the genera Noctacula andMesodinium. During bloom conditions, singlecelled organisms can cause the surface water tobecome red. Toxic dinoflagellate blooms turnred only when a certain density is reached.Individual toxic dinoflagellate cells may actuallybe most dangerous during the early part ofbloom when the red color is less likely toappear. Red coloration often occurs in patchescreated by winds and water currents passingthrough the area. Shellfish left in the wake ofthese moving poisonous patches may remaintoxic long after evidence of the algae bloom haspassed. Thus, water color alone is not a consis-tent indicator of PSP toxicity. To emphasize thispoint, none of the five PSP outbreaks in Kodiakin 1993 were preceded by a red tide. However,if a red tide is in progress, do not eat theshellfish! You may not know what is causing thered coloration.
Is shellfish purchased at a seafood retailersafe to eat?
Yes. Shellfish sold for human consumption mustmeet the Food and Drug Administration stan-dard of less than 80 ug of PSP toxin per 100grams of shellfish tissue. Alaska regulationsrequire regular monitoring of commerciallyharvested shellfish or batch certification thatrequires each commercially harvested or farmgrown batch of shellfish to pass the PSP testprior to market.
Are there some clam beaches in Alaskacertified to be free from PSP toxin?
No. Unlike other west coast states, Alaska doesnot certify recreational beaches for evidence ofPSP toxin. The term “certified beach” is used inAlaska, but a certified beach is one that haspassed a fecal coliform test. This test certifies abeach free from sewage caused pollution andindicates the shellfish are free of human patho-gens like cholera or hepatitis.
Truths andMythsabout PSP
15
Can I test for PSP in shellfish by chewing asmall piece of shellfish tissue and see if Ifeel tingling in my lips? If no tingling ornumbness occurs, is the shellfish OK to eat?
No. Only a mouse bioassay is approved by theU.S. Food and Drug Administration for detectionof PSP toxins. The test procedure first extractsPSP toxins from 150 grams of shellfish tissues.The extract is injected into 3 Swiss Websterstrain white mice 18-23 grams in weight. Theamount of time required for the mice to die isrecorded then converted to micrograms (ug) oftoxin by substitution into a prescribed math-ematical formula.
Chewing on a small piece of shellfish gives youno clue as to the PSP dosage in the tissue. Inaddition, PSP toxins in an acid pH environmentundergo chemical transformations that mayproduce more potent toxins than originallyfound in the shellfish. Since your mouth has anearly neutral pH, the toxins in your mouthmay not have the potency as the toxins thatare formed in acidic conditions of yourstomach. With data collected during recentoutbreaks, the Alaska Department of Epidemiol-ogy found evidence of toxin transformations inthe digestive tract of humans. The amount ofchange in PSP toxicity caused by these transfor-mations has not been confirmed and requiresadditional research.
Is my risk of getting PSP reduced if I digclams in an area where there is an ongoingcommercial fishery?
It depends. In the Cook Inlet region, PSP hasnot been a problem with razor clam harvesting.During the razor clam fishery for example,commercial harvesters submit a sample for PSPanalysis at every other tidal change. The AlaskaDepartment of Environmental Conservation thenfills in the remainder of the sampling schedule.This massive testing program has not found PSPlevels that exceed the FDA standard. The sameis true for the littleneck clam fishery inKachemak Bay. However, reliance on commer-cial fishery sampling has a major drawbacksince you do not have immediate knowledge ofthe commercial fishery PSP test results.
Shellfish from other locations around the state—Southeast Alaska, Prince William Sound, Kodiak,and the Aleutians; have PSP toxin problems.Commercial harvest of shellfish in these areasrequires certification of the harvested batchbefore marketing. Again, as a personal useharvester, you do not have access to the PSPtest results.
Does cleaning the intestinal contents of theshellfish make them safer to eat?
Sometimes. The digestive tract of the shellfishis the first tissue to accumulate PSP toxin fromthe food they consume, and cleaning theintestinal contents can reduce your risk if doneduring the early part of the toxic bloom. Theproblem, however, is that you have no indica-tion of how long the shellfish have been con-suming the toxic algae. After initial consumptionby the shellfish, the toxin distributes to othertissues, and the level of toxicity these othertissues achieve depends on a number of factors.Butter clams store highly toxic forms of toxins intheir siphon, the part most often eaten. Alongwith the intestinal contents the most toxic tissuestend to be gonad, siphon, foot, mantle, and gills.Several articles in this publication provideadditional information of tissue accumulation.
Does cooking eliminate PSP from shellfish?
No. PSP toxins are heat stable. Even whenpressure cooked at a temperature of 250oF for 15minutes, PSP remains toxic.
PSP: The Bacterial Connectionreferences continued from p. 13
Doucette, G.J. and C.G. Trick. 1995. Characterization of bacteria associatedwith different isolates of Alexandrium tamarense. Pages 33-38, in P.Lassus, G. Arzul, E. Erard, P. Gentien, and C. Marcaillou, editors. HarmfulAlgal Blooms. Technique et Documentation - Lavoisier, Intercept Limited.
Doucette, G.J. 1995. Interactions between bacteria and harmful algae: areview. Natural Toxins 3:65-74.
Kodama, M., T. Ogata, and S. Sato. 1988. Bacterial production ofsaxitoxin. Agriculture and Biological Chemistry. 52:1075-1077.
Kodama, M., T. Ogata, S. Sakamota, S. Sato, T. Honda, and T. Miwatani.1990. Production of paralytic shellfish toxins by a bacterium Moraxellasp. isolated from Protogonyaulax tamarensis. Toxicon 28:707:14.
Neal, R.A. 1967. Fluctuations in the levels of paralytic shellfish toxin infour species of lamellibranch molluscs near Ketchikan, Alaska, 1963-1965. Ph.D. Dissertation, University of Washington, Seattle, WA.pp. 1964
Schantz, E.J. and H.W. Magnussen. 1964. Observations of the origin ofparalytic poison in Alaska butter clams. Journal of Protozoology 11:239-242.
Silva, E.S. and I. Sousa. 1981. Experimental work on the dinoflagellatetoxin production. Arq. Inst. Nac. Sau´de 6:381-387.
Sparks A.D. 1966. Physiological ecology of the causative organismsincluding mechanisms of toxin accumulation in shellfish. pages 10-11,in W. Felsing (ed) Proceedings of Joint Sanitation Seminar on NorthPacific Clams. Alaska Department of Health and Welfare and U.S. Dept.of Health, Education, Welfare and Public Health Service.
Zimmerman, S.T. and R.S. McMahon. 1976. Paralytic shellfish poisoningin Tenakee, Southeastern Alaska: a possible cause. Fisheries Bull. (U.S.)74:679-680.
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The information presented below represents anupdate of information presented in a previouslypublished article (Gessner and Middaugh, Am JEpidemiol 1995;141:766-70). Persons interestedin further detail, including methodology, shouldconsult this article.
Between 1973 and 1994, 66 outbreaks ofparalytic shellfish poisoning occurred in Alaska,involving 143 ill persons. Of the 143 ill persons,the most common symptom was paresthesiasincluding perioral or extremity numbness ortingling (n=137). Other common symptomsincluded nausea or vomiting in 57 persons,trouble with balance in 39, dizziness in 37,shortness of breath in 35, a floating sensation in33, dry mouth in 23, difficulty seeing in 19,difficulty talking in 17, diarrhea in 10, anddifficulty swallowing in 10. Eight persons hadparalysis of a limb, eight required mechanicalventilator support, and two died. The time fromingestion of shellfish to illness onset rangedfrom 5 minutes to 11 hours (most commonly, 1hour). The time from illness onset until resolu-tion of symptoms ranged from 30 minutes to 8hours (most commonly, 8 hours). The majorityof persons had cooked their shellfish beforeeating it (76%).
Most outbreaks occurred during May and Junewith a smaller number during July (79%) (Figure1). However, outbreaks occurred during everymonth except November and December. Among61 outbreaks where the shellfish species wasknown, 57% involved butter clams (Saxidomus
giganteus); 30% involvedmussels (Mytilis edulis orcalifornianus); 13%involved cockles(Clinocardium nuttalli);and 5% each involvedrazor clams (Siliquapatula) or littleneckclams (Protothacastaminea); some out-breaks involved morethan one species.
For 1979-92, we deter-mined the location ofoutbreaks (Figure 2). Nooutbreaks occurred northof the Aleutian Chain.Most outbreaks occurredon Kodiak Island, thesouthern edge of theeastern half of theAleutian Islands, and inSoutheastern Alaska.Interestingly, no out-breaks have resulted
from eating shellfish collected from Cook Inlet,including Clam Gulch, and only one outbreakhas resulted from eating clams collected fromPrince William Sound, on Montague Island.
To evaluate the historical trends of paralyticshellfish poison levels in Alaska shellfish, weanalyzed records from the Alaska Department ofEnvironmental Conservation for all shellfishtested which had detectable paralytic shellfishpoison (>39 ug/100 gm tissue) during July 1982-February 1992. These records roughly corre-sponded with data from outbreaks and showedthat the mean paralytic shellfish poison levelvaried by month and shellfish type and that thehighest toxin levels occurred among musselsand butter clams during May and June. All typesof shellfish tested, except razor clams, had atleast one sample with detectable levels duringthe winter (December-February).
CommentAlthough suspected previously, a recent investi-gation provides evidence that most cases ofparalytic shellfish poisoning go unreported(Alaska Division of Public Health, unpublisheddata). Cases of paralytic shellfish poisoning aresentinel events, signaling public health provid-ers to warn local residents about the increaseddanger from eating shellfish. For this reason,persons who experience symptoms of paralyticshellfish poisoning, even if they only experiencenumbness or tingling, should immediatelyreport their symptoms to a medical provider.Medical providers, in turn, should immediatelyreport all suspected cases of paralytic shellfishpoisoning to the Alaska Section of Epidemiology.
The data presented above indicates that themost dangerous shellfish consumption involveseating mussels or butter clams collected fromsouth of the Aleutian chain during May, June, orJuly. Although less dangerous, outbreaks havealso occurred with razor clams, cockles, andlittleneck clams. Additionally, outbreaks haveoccurred during all months of the year exceptNovember and December. It is also important torecognize that saxitoxin and its analogues areheat stable toxins. Thus, unlike many othershellfish-borne illnesses, paralytic shellfishpoisoning may occur even when eating cookedshellfish. While some persons believe siphonremoval prevents illness, evidence indicates thatsufficient toxin exists in the remainder of theshellfish to cause symptoms. Persons whoharvest shellfish, including recreational andsubsistence users, should familiarize themselveswith the epidemiology of paralytic shellfishpoisoning to minimize their risk of illness.
Epidemiologyof ParalyticShellfishPoisoningOutbreaks inAlaskaDr. Brad Gessner,Section ofEpidemiology,Alaska Departmentof Health andSocial Services
Symptoms of 143 people withparalytic shellfish poisoning,Alaska, 1973-94
Symptom Number
Paresthesias (tingling on skin) 113Perioral (lip) numbness 64Perioral (lip) tingling 61Nausea 45Extremity numbness 43Extremity tingling 39Vomiting 34Weakness 33Ataxia (immobility) 32Shortness of breath 29Dizziness 28Floating sensation 24Dry mouth 23Diplopia (double vision) 19Dysarthria (difficulty speaking) 16Diarrhea 10Dysphagia (difficulty swallowing) 6Limb paralysis 4
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Case Histories:Paralytic ShellfishPoisoning
Case 1Within one hour after eating50 roasted mussels, a 28-year-old male Kodiak residentdeveloped perioralparesthesias, nausea, andvomiting followed by head-ache, and difficulty talking,swallowing, and walking.Shortly after presenting to theKodiak Island Hospital hehad a respiratory arrest. Thepatient was rapidly incubatedand placed on mechanicalventilation. A neurologicexamination shortly after therespiratory arrest suggestedthe patient did not havecortical functioning andconsideration was given topronouncing him dead. Theclinicians caring for the patient, however,recognized that the symptoms were consistentwith paralytic shellfish poisoning and main-tained supportive therapy. Several hours laterthe patient regained consciousness and within24 hours had complete symptom resolution.
Case 2Within 1 hour of eating at least 12 raw andcooked mussels, a 61-year-old female OldHarbor resident developed paresthesias, vomit-ing, weakness, and difficulty walking. Soon afterpresentation at the local health clinic shesuffered a respiratory arrest. Because no trainedpersonnel or equipment for endotrachealintubation were available, communityhealth workers supported the patientwith bag and mask ventilation.When emergency medical techni-cians arrived for air transport toKodiak, the patient had nopulse or voluntary respirations.At the Kodiak Island Hospital,a cardiac examination sug-gested her heart had stoppedworking. Despite vigorous
resuscitative efforts, she was pronounced deadapproximately six hours after she had consumedmussels.
CommentThese two cases illustrate the potential severityof paralytic shellfish poisoning. Patient 1
Figure 1:
Figure 2: Location of paralytic shellfish poisoning outbreaks; Alaska, 1973-92★ indicates ≥ 1 outbreak
Outbreaks of paralytic shellfish poisoning(n=66), by month; Alaska, 1973-94
2 32 2
2321
8
2 2 10 0
January February March April May June July August September October November December
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ParalyticShellfishPoisoningIn TheNorthPacific:TwoHistoricalAccountsandImplicationsfor TodayRobert Fortuine,M.D.Excerpt from“Chills andFever”,published byUniversity ofAlaska Press
The Natives of Alaska were exposed to severaltypes of poisonous substances in their naturalenvironment. Although general experience andcultural taboos protected them from frequentencounters with these hazards, illness and deathcould result from accidental (or sometimesintentional) exposure.
Paralytic shellfish poisoning, or PSP, is causedby the ingestion of a powerful toxin that isproduced by severe species of plankton calleddinoflagellates. These plankton sometimes“bloom” and are ingested by certain bivalvemollusks, such as mussels and razor clams.When the latter in turn are eaten by humans, asevere illness may result. The disease is charac-terized by numbness and tingling around themouth, vomiting, diarrhea, and double vision,followed in severe cases by respiratory paralysisthat may lead to death. This problem was firstidentified in the north Pacific nearly two hun-dred years ago and still claims periodic victims(Fortuine 1975b.)
What was undoubtedly an episode of severePSP occurred in southeastern Alaska in July1799, although early accounts differ on the date.Aleksandr Baranov himself, the chief manager ofthe newly formed Russian-American Company,has left a description of this tragic event, eventhough he was not personally a witness. A largeparty of Aleut hunters under his command hadleft the new fort on Sitka Island and were ontheir way back to Kodiak in their skin boats,when they stopped for the night at a placecalled Khutznov Strait, later called Peril Strait tocommemorate the event. Although well suppliedwith provisions, the Natives could not resisteating some of the small, black mussels thatwere abundant in the area. Two minutes laterabout half the party experienced nausea and felta dryness in the throat. By the end of two hours,says the account, about a hundred hunters haddied. Some were saved, according to Baranov,by taking a mixture of gunpowder, tobacco, andspirits to induce vomiting. So far so good, butthe chief manager goes on to describe how theillness then became infectious and others diedwithout having eaten the mussels at all (Baranovin Tikhmenev 1979, 110-11; Khlebnikov 1973,26-27).
The unique account of a Native witness—aKoniag named Arsenti—was preserved byHeinrich Johan Holmberg many years later(1985, 43):
“When we found ourselves in Pogibshiiproliv (Peril Strait), we turned to eatingmussels (Mytilis) because of a shortage offresh fish. They must have been poisonousat this time of year for a few hours latermore than half of our men died. Even I wasnear death, but remembering my father’sadvice, to eat smelt (korushki) at suchtimes, I vomited and recovered my health.”
Arsenti’s version is interesting because it showsthat he knew mussels were poisonous in certainseasons of the year, and also knew of a tradi-tional remedy, both of which point to previousexperience with the disease.
The account of the same episode by Davydov(1977, 177) a few years later sheds some furtherlight. According to him the Koniag were wellacquainted with shellfish poisoning and knewthat the mollusks could be harmless at sometimes and poisonous at others. In describing theevents at Peril Strait (which he incorrectly datesin 1797), he recalled that the party camped atthe mouth of a stream where there were manyshellfish on both banks. Only those from thebank where there was no seaweed coveringthem caused illness. Within a half hour of eatingthe mussels a Chugach Eskimo had died,followed shortly by the death of five Koniag.According to Davydov, some eighty personsdied that day. All who immediately ate sulfur,rotting fish, tobacco, or gunpowder survived,although some still had tingling sensations inthe skin several years later. Davydov heard thatpepper boiled in water was also an effectiveremedy, although no one seems to have tried itat the time. He also asserted that those whowere affected felt some relief with the ebb tide.
The disaster at Peril Strait was an unforgettableone but certainly not unique. Veniaminov (1984,364) mentioned that the Aleuts knew that clamsand mussels were sometimes poisonous fromMay to September, while Holmberg (1985, 42-43) indicated that shellfish poisoning was wellknown in Kodiak in earlier times.
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Have you seen:• discolored ocean, bay or estuary waters?• unusual behavior or illness displayed by a group of fish, birds, or mammals?• an extensive bird, mammal, or fish kill?
If your answer is yes, call Sea Watch at 1-800-731-1312 and report your observations.
The Department of Environmental Conservation’s (DEC ) Division of Environmental Health is urging you to callthis information so that it can be used with marine toxin data to help forecast toxic events. These forecasts couldhelp with public health notices regarding the possibility of toxic shellfish or crab, and assist the department inmonitoring commercial crab harvests for possible PSP.
Marine toxins, such as PSP and domoic acid, are produced under certain environmental conditions by marinephytoplankton—the source of “red tides” sometimes observed. The toxins may be concentrated in the bodies offilter-feeding shellfish and in the viscera or guts, of crab and can thus become a public health hazard.
When you call, the department needs to know the exact location of your sighting, in detail if possible, especiallylatitude/longitude, loran, or by landmark. They would also like you to collect a quart or more of the water in aclean container and refrigerate it. When you call they will give you instructions on what to do with it.
Sea Watch
ReferencesDavydov, G.I. 1977. Two voyages to RussianAmerica, 1802-1807. Translated by C. Berne. Ed.R.A. Pierce. Kingston, Ontario: Limestone Press.
Fortuine, R. 1975b. Paralytic shellfish poisoningin the North Pacific: Two historical accounts andimplications today. Alaska Medicine 17(5):71-76.
Holmberg, H. 1985. Holmberg’s ethnographicsketches. Ed. Marvin W. Falk. Translated by F.Jaensch. The Rasmuson Library HistoricalTranslation Series. Vol. 1. Fairbanks: Universityof Alaska Press.
Khlebnikov, K.T. 1973. Baranov: Chief Managerof the Russian colonies in American. Translatedby C. Bearne. Ed. R.A. Pierce. Kingston, Ontario:Limestone Press.
Tikhmenev, P.A. 1979. A history of the RussianAmerican Company. Volume 2 documents.Pertiod 1783-1807. Translated by D. Krenov. Ed.R.A. Pierce and A.S. Donnelly. Kingston,Ontario: Limestone Press.
Veniaminov, I. 1984. Notes on the islands of theUnalaska District. Translated by L.T. Black andR.H. Geoghegan. Ed. R.A. Pierce. Kingston,Ontario: Limestone Press.
Epidemiologyof Paralytic
ShellfishPoisoning
Outbreaks inAlaskacontinued
continued from p. 17
survived only because he was able to findmedical assistance before he had a respiratoryarrest and because of the clinical acuteness ofthe health care providers caring for him. Thiscase emphasizes the need for health careproviders to recognize the symptoms of paralyticshellfish poisoning and, when it is suspected, tomaintain respiratory support regardless ofadverse neurologic findings. Case 2 died despitereceiving appropriate medical care before herrespiratory arrest. It is possible that she died of acardiac arrhythmia rather than respiratory arrest,a recognized complication when exceptionallyhigh amounts of toxin have been ingested. Bothof these patients ate mussels, the shellfishtraditionally associated with the highest toxinlevels; collecting during May, the month whichusually has the highest toxin levels; from KodiakIsland, a location which has been the site ofseveral previous outbreaks. This raises thepossibility that culturally appropriate educationcould have prevented these outcomes.
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