Paralytic Shellfish Poisoning and Neurotoxic Shellfish Poisoning

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Paralytic Shellfish Poisoning and Neurotoxic Shellfish Poisoning Associated With Bivalves During Harmful Algal Bloom Events

 There are dangerous effects of harmful algal blooms (HAB) in marine and freshwater ecosystems, like the one seen recently along the Florida coastline. With these widespread occurrences comes dangerous toxins that can cripple an ecosystem and become harmful on not only the marine and freshwater animals but can also affect the humans that consume food from these contaminated waters. The HAB events within marine environments are caused by certain types of algae that produce toxins that can cause Paralytic Shellfish Poisoning (PSP) or Neurotoxic Shellfish Poisoning (NSP).  Saxitoxin is the main cause of paralytic shellfish toxins (PST), although over 50 different compounds have been identified as being involved in toxin production (Costa, 2016). PST has been linked to at least nine different dinoflagellates with seven species producing the toxin (Costa, 2016).

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With NSP a neurotoxin called brevetoxin is the main culprit which is produce by Karenia brevis, the species that has been linked to Florida’s red time HAB events (Wolny, et al., 2015). During HAB events these toxins can be produced and lead to fish kills, which is a good indicator that the toxin could be present. Larger commercially caught fish that feed on organisms that are vectors of the toxin can be included in the fish kills, and there has been historical reports that birds, whales, and domestic animals can be affected by consuming fish that contain the saxitoxin or neurotoxin brevetoxin (Wolny, et al., 2015). Bivalves such as mussels, clams, and oysters are vectors of the toxins as they are filter-feeders and pose the most danger in human consumption, although fish that are eaten during fish kills still can contain the toxins within their bodies.

 

Identification Techniques Used in Finding PST and Brevetoxin

  Some different lab techniques have been used to identify PST and the neurotoxin brevetoxin that occur during HAB events. The most common technique used over the past few decades in the detection of PST has been a mouse bioassay (MBA). This technique involves taking infected tissue from bivalves, grounding it up and mixing with an acidic agent to extract the toxin. Once the extracted toxin is filtered it can be injected into a mouse. The toxicity is then measured by the amount of toxin that it takes to kill a 20g mouse, which has earned the measurement the name “mouse units” (Alonso, et al., 2016).

Recent research has been done to determine simpler and more cost-effective methods to identify the presence of PST. Techniques such as qPCR to identify specific genes for saxitoxin, liquid chromatography with fluorescence, and hydrophilic interaction liquid chromatography with tandem mass spectrometry have been used to identify the presence and concentration of PST( (Penna, et al., 2015)). Based on research in identifying the presence and concentration of brevetoxin, the MBA and enzyme-linked immunosorbent assay (ELISA) using goat anti-brevetoxin antibodies are the methods still being most commonly used (Baden, et al., 2002).

 

How the Toxins Work

PST and brevetoxins are neurotoxins that accumulate in the digestive tracts of bivalves. When consumed by humans, the neurotoxins block voltage-gated sodium (Na) channels. Toxins that affect the Na channels in the central and peripheral nervous systems can keep neurons from firing. The toxins can also affect the dendrites and synapses. This is what leads the neurological deficits associated with PSP. There are more than 50 tetrahydropurine toxins related to saxitoxin that cause PSP, with varying levels of toxicity. Besides saxitoxin (STX), some of the more potent toxins are neoSTX, dcSTX, and GTX1. The legal limit of these toxins in bivalve meat is 4 mouse units (800µg)/kg of meat. In a study on these toxins effect on different Na channels, it was discovered that the neoSTX toxin had a very high toxic potency in most of the Na channels in the central and peripheral nervous systems (Alonso, et al., 2016).

Effects on Human Population

 The toxins produced during HAB events can be disastrous on marine ecosytstems. The effects the human population both economically and physically. The genera responsible for producing saxitoxin and other related toxins are Alexandrium, Gymnodinium, and Pyrodinium, are common in HAB events. They can harm fish that feed on phytoplankton leading to major fish kills that can harm fisheries. The major concern for humans is that bivalves such as oysters, mussels, and clams can contain the toxins produced by these dinoflagellates.

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Humans that consume the toxins within these bivalves can have adverse health issues. PSP can occur within a few hours of consuming clams, oysters, or mussels contaminated with saxitoxin. Patients have been reported to have experienced gastrointestinal discomfort and neurological symptoms, such as tingling in extremities or paresthesias, loss of full body control (ataxia), difficulty swallowing, and changes to mental status. Most patients will recover but some cases can lead to respiratory paralysis, leading to asphyxiation and death (Hurley, Wolterstorff, & MacDonald, 2014). Currently, there is no antidote for PSP, and patients are usually given intravenous fluids and are put on a respirator (Silver, 2006). Only a few milligrams of saxitoxin or related toxin is needed to cause death in patients.

Pufferfish, which are most known to have a risk of having tetrodotoxin (TTX) are one fish that can also contain saxitoxin in the edible tissues. Pufferfish have a high affinity for toxins than allow them to survive while carrying toxic levels of saxitoxin. Consuming bivalves that contain the neurotoxin brevetoxin causes severe symptoms such as nausea, diarrhea, head and muscle aches, dizziness, and reversal of hot/cold sensation. These symptoms typically occur a few hours after consumption but are typically not fatal like PSP (Wolney, et al., 2015).

Case Studies in the United States

 PSP cases have been widely reported around the globe, but few have been reported along the United States coastlines. One of the first case studies in the U.S. was in San Francisco in 1927. Over 100 cases of what would be determined as PSP were reported with some of the cases being fatal. At this time, there was no knowledge that algae could cause this type of sickness as most cases of foodborne illness involving bivalves was linked to bacteria. What followed was 10 years of research on a few other cases of PSP before it was discovered that Alexandrium catanella was the reason behind the outbreak of illness in San Francisco (Silver, 2006).

 A more recent case of PSP was reported in Alaska in 2011. Up to 21 people consumed cockles or bivalves that contained saxitoxin and were admitted to hospitals with symptoms related with PSP. All the cases involved noncommercially acquired cockles, mussels, or clams. The epidemiologists assigned to investigate the outbreak discovered high levels of saxitoxin in leftover mussels and cockles that were caught by the patients. In the figure below, you can see that a few of the patients consumed foods that had toxin levels over 1000µg/100g of meat, enough to be fatal:

(Paralytic Shellfish Poisoning, 2011)

 Florida has had many red tide HAB events along its western coast caused by Karenia brevis. In 2007-2008, the eastern coast had a HAB event that lasted 4 months, the longest red tide event on the east coast (as of 2015). Despite high concentrations of concentrations of brevetoxin in tested shellfish, there were no NSP illnesses reported. One thing that was discovered during this study was that in area where shellfish tested above the legal limit for brevetoxin, it took clams an average of 8 days to eliminate brevetoxin and oysters and average of 30 days to eliminate brevetoxin (Wolny, et al., 2015).

Summary

 HAB events that occur around coastal areas can have a serious impact on food safety. Small amounts of brevetoxin can lead to serious health impacts and small amounts of saxitoxin or related toxins can prove fatal. Bivalves that contain toxins are especially dangerous because they are filter-feeders than can contain the toxins in their digestive tract. The toxins are present even after cooking and do not respond to irradiation. Due to their ability to block Na channels in the central and peripheral nervous systems they can cause major implications in the body’s ability to function. There is no antidote to the toxins that are present during a HAB event. The best preventative measure to consuming these dangerous toxins is to only eat commercially acquired shellfish and never eat shellfish from an area with a HAB event. Toxins can still be present in bivalves just after a HAB event.

Bibliography

Paralytic Shellfish Poisoning and Neurotoxic Shellfish Poisoning Associated With Bivalves During Harmful Algal Bloom Events

 There are dangerous effects of harmful algal blooms (HAB) in marine and freshwater ecosystems, like the one seen recently along the Florida coastline. With these widespread occurrences comes dangerous toxins that can cripple an ecosystem and become harmful on not only the marine and freshwater animals but can also affect the humans that consume food from these contaminated waters. The HAB events within marine environments are caused by certain types of algae that produce toxins that can cause Paralytic Shellfish Poisoning (PSP) or Neurotoxic Shellfish Poisoning (NSP).  Saxitoxin is the main cause of paralytic shellfish toxins (PST), although over 50 different compounds have been identified as being involved in toxin production (Costa, 2016). PST has been linked to at least nine different dinoflagellates with seven species producing the toxin (Costa, 2016).

With NSP a neurotoxin called brevetoxin is the main culprit which is produce by Karenia brevis, the species that has been linked to Florida’s red time HAB events (Wolny, et al., 2015). During HAB events these toxins can be produced and lead to fish kills, which is a good indicator that the toxin could be present. Larger commercially caught fish that feed on organisms that are vectors of the toxin can be included in the fish kills, and there has been historical reports that birds, whales, and domestic animals can be affected by consuming fish that contain the saxitoxin or neurotoxin brevetoxin (Wolny, et al., 2015). Bivalves such as mussels, clams, and oysters are vectors of the toxins as they are filter-feeders and pose the most danger in human consumption, although fish that are eaten during fish kills still can contain the toxins within their bodies.

 

Identification Techniques Used in Finding PST and Brevetoxin

  Some different lab techniques have been used to identify PST and the neurotoxin brevetoxin that occur during HAB events. The most common technique used over the past few decades in the detection of PST has been a mouse bioassay (MBA). This technique involves taking infected tissue from bivalves, grounding it up and mixing with an acidic agent to extract the toxin. Once the extracted toxin is filtered it can be injected into a mouse. The toxicity is then measured by the amount of toxin that it takes to kill a 20g mouse, which has earned the measurement the name “mouse units” (Alonso, et al., 2016).

Recent research has been done to determine simpler and more cost-effective methods to identify the presence of PST. Techniques such as qPCR to identify specific genes for saxitoxin, liquid chromatography with fluorescence, and hydrophilic interaction liquid chromatography with tandem mass spectrometry have been used to identify the presence and concentration of PST( (Penna, et al., 2015)). Based on research in identifying the presence and concentration of brevetoxin, the MBA and enzyme-linked immunosorbent assay (ELISA) using goat anti-brevetoxin antibodies are the methods still being most commonly used (Baden, et al., 2002).

 

How the Toxins Work

PST and brevetoxins are neurotoxins that accumulate in the digestive tracts of bivalves. When consumed by humans, the neurotoxins block voltage-gated sodium (Na) channels. Toxins that affect the Na channels in the central and peripheral nervous systems can keep neurons from firing. The toxins can also affect the dendrites and synapses. This is what leads the neurological deficits associated with PSP. There are more than 50 tetrahydropurine toxins related to saxitoxin that cause PSP, with varying levels of toxicity. Besides saxitoxin (STX), some of the more potent toxins are neoSTX, dcSTX, and GTX1. The legal limit of these toxins in bivalve meat is 4 mouse units (800µg)/kg of meat. In a study on these toxins effect on different Na channels, it was discovered that the neoSTX toxin had a very high toxic potency in most of the Na channels in the central and peripheral nervous systems (Alonso, et al., 2016).

Effects on Human Population

 The toxins produced during HAB events can be disastrous on marine ecosytstems. The effects the human population both economically and physically. The genera responsible for producing saxitoxin and other related toxins are Alexandrium, Gymnodinium, and Pyrodinium, are common in HAB events. They can harm fish that feed on phytoplankton leading to major fish kills that can harm fisheries. The major concern for humans is that bivalves such as oysters, mussels, and clams can contain the toxins produced by these dinoflagellates.

Humans that consume the toxins within these bivalves can have adverse health issues. PSP can occur within a few hours of consuming clams, oysters, or mussels contaminated with saxitoxin. Patients have been reported to have experienced gastrointestinal discomfort and neurological symptoms, such as tingling in extremities or paresthesias, loss of full body control (ataxia), difficulty swallowing, and changes to mental status. Most patients will recover but some cases can lead to respiratory paralysis, leading to asphyxiation and death (Hurley, Wolterstorff, & MacDonald, 2014). Currently, there is no antidote for PSP, and patients are usually given intravenous fluids and are put on a respirator (Silver, 2006). Only a few milligrams of saxitoxin or related toxin is needed to cause death in patients.

Pufferfish, which are most known to have a risk of having tetrodotoxin (TTX) are one fish that can also contain saxitoxin in the edible tissues. Pufferfish have a high affinity for toxins than allow them to survive while carrying toxic levels of saxitoxin. Consuming bivalves that contain the neurotoxin brevetoxin causes severe symptoms such as nausea, diarrhea, head and muscle aches, dizziness, and reversal of hot/cold sensation. These symptoms typically occur a few hours after consumption but are typically not fatal like PSP (Wolney, et al., 2015).

Case Studies in the United States

 PSP cases have been widely reported around the globe, but few have been reported along the United States coastlines. One of the first case studies in the U.S. was in San Francisco in 1927. Over 100 cases of what would be determined as PSP were reported with some of the cases being fatal. At this time, there was no knowledge that algae could cause this type of sickness as most cases of foodborne illness involving bivalves was linked to bacteria. What followed was 10 years of research on a few other cases of PSP before it was discovered that Alexandrium catanella was the reason behind the outbreak of illness in San Francisco (Silver, 2006).

 A more recent case of PSP was reported in Alaska in 2011. Up to 21 people consumed cockles or bivalves that contained saxitoxin and were admitted to hospitals with symptoms related with PSP. All the cases involved noncommercially acquired cockles, mussels, or clams. The epidemiologists assigned to investigate the outbreak discovered high levels of saxitoxin in leftover mussels and cockles that were caught by the patients. In the figure below, you can see that a few of the patients consumed foods that had toxin levels over 1000µg/100g of meat, enough to be fatal:

(Paralytic Shellfish Poisoning, 2011)

 Florida has had many red tide HAB events along its western coast caused by Karenia brevis. In 2007-2008, the eastern coast had a HAB event that lasted 4 months, the longest red tide event on the east coast (as of 2015). Despite high concentrations of concentrations of brevetoxin in tested shellfish, there were no NSP illnesses reported. One thing that was discovered during this study was that in area where shellfish tested above the legal limit for brevetoxin, it took clams an average of 8 days to eliminate brevetoxin and oysters and average of 30 days to eliminate brevetoxin (Wolny, et al., 2015).

Summary

 HAB events that occur around coastal areas can have a serious impact on food safety. Small amounts of brevetoxin can lead to serious health impacts and small amounts of saxitoxin or related toxins can prove fatal. Bivalves that contain toxins are especially dangerous because they are filter-feeders than can contain the toxins in their digestive tract. The toxins are present even after cooking and do not respond to irradiation. Due to their ability to block Na channels in the central and peripheral nervous systems they can cause major implications in the body’s ability to function. There is no antidote to the toxins that are present during a HAB event. The best preventative measure to consuming these dangerous toxins is to only eat commercially acquired shellfish and never eat shellfish from an area with a HAB event. Toxins can still be present in bivalves just after a HAB event.

Bibliography

  • Alonso, E., Alfonso, A., Vieytes, M. R., & Botana, L. M. (2016). Evaluation of toxicity equivalent factors of paralytic shellfish poisoning toxins in seven human sodium channels types by an automated high throughput electrophysiology system. Archives Of Toxicology90(2), 479–488. https://doi.org/10.1007/s00204-014-1444-y
  • Baden, D. G., Bourdelais, A., Naar, J., Tomas, C., Kubanek, J., Whitney, P. L., Flewelling, L.(2002). A Competitive ELISA to Detect Brevetoxins from Karenia brevis (Formerly Gymnodinium breve) in Seawater, Shellfish, and Mammalian Body Fluid. Environmental Health Perspectives, (2), 179. Retrieved from https://ezproxy.mtsu.edu/login?url=http://search.ebscohost.com/login.aspx?direct=true&db=edsjsr&AN=edsjsr.3455377&site=eds-live&scope=site
  • Costa, P. R. (n.d.). Impact and effects of paralytic shellfish poisoning toxins derived from harmful algal blooms to marine fish. Fish and Fisheries17(1), 226–248. https://doi.org/10.1111/faf.12105
  • Hurley, W., Wolterstorff, C., & MacDonald, R. (2014). Paralytic Shellfish Poisoning: A Case Series. Western Journal of Emergency Medicine: Integrating Emergency Care with Population, 378-381.
  • Kacem, I. ( 1 ), Papiol, G. G. ( 2,5 ), De La Iglesia, P. ( 2 ), Diogène, J. ( 2 ), Hajjem, B. ( 3 ), & Bouaïcha, N. ( 4 ). (n.d.). Comparative toxicity and paralytic shellfish poisoning toxin profiles in the mussel mytilus galloprovincialis and the oyster crassostrea gigas collected from a mediterranean lagoon in tunisia: A food safety concern. International Journal of Food Properties18(5), 1075–1085. https://doi.org/10.1080/10942912.2014.913179
  • NEUROTOXIC SHELLFISH POISONING — Florida. (1974). Morbidity and Mortality, 23(12), 115-115. Retrieved from http://www.jstor.org/stable/44073405
  • Paralytic shellfish poisoning — southeast Alaska, May–June 2011. (2011). MMWR. Morbidity And Mortality Weekly Report60(45), 1554–1556. Retrieved from https://ezproxy.mtsu.edu/login?url=http://search.ebscohost.com/login.aspx?direct=true&db=mnh&AN=22089968&site=eds-live&scope=site
  • Penna, A., Perini, F., Dell’Aversano, C., Capellacci, S., Tartaglione, L., Grazia Giacobbe, M., . . . Scardi, M. (2015). The sxt Gene and Paralytic Shellfish Poisoning Toxins as Markers for the Monitoring of Toxic Alexandrium Species Blooms. Environmental Science Technology, 14230-14238.
  • Shin, C., Jang, H., Jo, H., Kim, H.-J., Kim, D.-S., & Hong, J.-H. (2017, July). Development and validation of an accurate and sensitive LC-ESI-MS/MS method for the simultaneous determination of paralytic shellfish poisoning toxins in shellfish and tunicate. Food Control, 77, 171-178.
  • Silver, M. W. (2006). Protecting Ourselves from Shellfish Poisoning. AMERICAN SCIENTIST, (4), 316. Retrieved from https://ezproxy.mtsu.edu/login?url=http://search.ebscohost.com/login.aspx?direct=true&db=edsbl&AN=RN190645150&site=eds-live&scope=site
  • Wolny, J. L., Scott, P. S., Tustison, J., & Brooks, C. R. (n.d.). Monitoring the 2007 Florida east coast Karenia brevis (Dinophyceae) red tide and neurotoxic shellfish poisoning (NSP) event. ALGAE30(1), 49–58. https://doi.org/10.4490/algae.2015.30.1.049
  • Yang, X. ( 1 ), Zhao, Z. ( 1 ), Nie, D. ( 1 ), Zhou, C. ( 1 ), Zhou, L. ( 2 ), Shi, X. ( 2 ), … Liu, H. ( 4 ). (n.d.). Development and validation of a liquid chromatography-tandem mass spectrometry method coupled with dispersive solid-phase extraction for simultaneous quantification of eight paralytic shellfish poisoning toxins in shellfish. Toxins9(7). https://doi.org/10.3390/toxins9070206

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