scholarly journals Changing Trends in Paralytic Shellfish Poisonings Reflect Increasing Sea Surface Temperatures and Practices of Indigenous and Recreational Harvesters in British Columbia, Canada

Marine Drugs ◽  
2021 ◽  
Vol 19 (10) ◽  
pp. 568
Author(s):  
Lorraine McIntyre ◽  
Aroha Miller ◽  
Tom Kosatsky
Keyword(s):  
British Columbia ◽  
Single Case ◽  
Indigenous Communities ◽  
Paralytic Shellfish Poisoning ◽  
Shellfish Poisoning ◽  
Quality Of Data ◽  
Paralytic Shellfish Toxins ◽  
Paralytic Shellfish ◽  
Phytoplankton Monitoring ◽  
High Concentrations

Paralytic shellfish poisoning (PSP) occurs when shellfish contaminated with saxitoxin or equivalent paralytic shellfish toxins (PSTs) are ingested. In British Columbia, Canada, documented poisonings are increasing in frequency based on 62 investigations identified from 1941–2020. Two PSP investigations were reported between 1941 and 1960 compared to 31 since 2001 (p < 0.0001) coincident with rising global temperatures (r2 = 0.76, p < 0.006). The majority of PSP investigations (71%) and cases (69%) were linked to self-harvested shellfish. Far more investigations involved harvests by indigenous communities (24%) than by commercial and recreational groups. Single-case-exposure investigations increased by more than 3.5 times in the decade 2011–2020 compared to previous periods. Clams (47%); mussels (26%); oysters (14%); scallops (6%); and, in more recent years, crabs (4%) were linked to illnesses. To guide understanding of self-harvesting consumption risks, we recommend collecting data to determine when PST-producing algae are present in high concentrations, improving the quality of data in online shellfish harvest maps to include dates of last testing; biotoxin testing results; and a description of bivalve species tested. Over reliance on toxin results in biomonitored species may not address actual consumption risks for unmonitored species harvested from the same area. We further recommend introducing phytoplankton monitoring in remote indigenous communities where self-harvesting is common and toxin testing is unavailable, as well as continuing participatory education about biotoxin risks in seafoods.

Foodborne and Waterborne Disease in Canada — 1980 Annual Summary

1987 ◽  
Vol 50 (5) ◽  
pp. 420-428 ◽  
Author(s):  
E. C. D. TODD
Keyword(s):  
British Columbia ◽  
Food Processing ◽  
Paralytic Shellfish Poisoning ◽  
Foodborne Disease ◽  
Shellfish Poisoning ◽  
Waterborne Disease ◽  
Paralytic Shellfish ◽  
Uremic Syndrome ◽  
Marine Food ◽  
First Time

Data on foodborne disease in Canada in 1980 are compared with those for 1979. A total of 759 incidents, comprising 621 outbreaks and 138 single cases, caused illnesses in 7,122 persons in 1980. Compared with 1979, fewer incidents but more cases occurred. Salmonella, Staphylococcus aureus, Clostridium perfringens and Bacillus cereus caused most illnesses. The main Salmonella serovars involved were S. typhimurium, S. heidelberg and S. enteritidis. Campylobacter and Citrobacter infections were reported for the first time. Seven episodes of paralytic shellfish poisoning occurred, more than twice the number in 1979. There were also 53 incidents and 100 cases of chemical origin; rancid compounds, extraneous matter and metals were the main chemicals involved. Unusual chemical problems included turkey contaminated with calcium chloride brine, antimony deliberately added to a beverage to induce sickness, ammonia-soaked frozen potato puffs, chocolates contaminated with phenol disinfectant and toluene in popcorn twists. There were nine deaths from salmonellosis, paralytic shellfish poisonings and hemolytic uremic syndrome. About 34% of incidents and 51% of cases were associated with meat and poultry. Vegetables, fruits, Chinese food, marine food and bakery products were also vehicles that contributed significantly to foodborne disease. Mishandling of food took place mainly in foodservice establishments (41.2% of incidents, 74.3% of cases), homes (15.8% of incidents, 6.0% of cases) and food processing establishments (10.1% of incidents, 8.7% of cases). Food processors were responsible for salmonellosis from turkey rolls (440 cases) and staphylococcal intoxication from cheese curds (62 cases) and many small outbreaks and single cases. Most incidents occurred in Ontario (43.9%) and British Columbia (21.7%), but on a 100,000 population basis, British Columbia recorded more incidents (6.2) than Nova Scotia and Yukon (both 4.5) and Ontario (3.9). Narrative reports of seven foodborne disease incidents are presented. Four incidents of waterborne disease were documented in 1980, the same number as in 1979. All were caused by bacterial agents, with Campylobacter and Salmonella responsible for most cases. Pseudomonas aeruginosa infected the skin of 10 persons in a whirlpool bath.

scholarly journals Prominent Human Health Impacts from Several Marine Microbes: History, Ecology, and Public Health Implications

2011 ◽  
Vol 2011 ◽  
pp. 1-15 ◽  
Author(s):  
P. K. Bienfang ◽  
S. V. DeFelice ◽  
E. A. Laws ◽  
L. E. Brand ◽  
R. R. Bidigare ◽  
...  
Keyword(s):  
Public Health ◽  
Paralytic Shellfish Poisoning ◽  
Health Impacts ◽  
Marine Cyanobacteria ◽  
Extensive Literature ◽  
Shellfish Poisoning ◽  
Marine Microbes ◽  
Fish Poisoning ◽  
Paralytic Shellfish ◽  
High Concentrations

This paper overviews several examples of important public health impacts by marine microbes and directs readers to the extensive literature germane to these maladies. These examples include three types of dinoflagellates (Gambierdiscusspp.,Karenia brevis, andAlexandrium fundyense), BMAA-producing cyanobacteria, and infectious microbes. The dinoflagellates are responsible for ciguatera fish poisoning, neurotoxic shellfish poisoning, and paralytic shellfish poisoning, respectively, that have plagued coastal populations over time. Research interest on the potential for marine cyanobacteria to contribute BMAA into human food supplies has been derived by BMAA's discovery in cycad seeds and subsequent implication as the putative cause of amyotrophic lateral sclerosis/parkinsonism dementia complex among the Chamorro people of Guam. Recent UPLC/MS analyses indicate that recent reports that BMAA is prolifically distributed among marine cyanobacteria at high concentrations may be due to analyte misidentification in the analytical protocols being applied for BMAA. Common infectious microbes (including enterovirus, norovirus,Salmonella,Campylobacter,Shigella,Staphylococcus aureus,Cryptosporidium, andGiardia) cause gastrointestinal and skin-related illness. These microbes can be introduced from external human and animal sources, or they can be indigenous to the marine environment.

scholarly journals Paralytic Shellfish Toxins (PST)-Transforming Enzymes: A Review

Toxins ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 344
Author(s):  
Mariana I. C. Raposo ◽  
Maria Teresa S. R. Gomes ◽  
Maria João Botelho ◽  
Alisa Rudnitskaya
Keyword(s):  
Harmful Algal Blooms ◽  
Algal Blooms ◽  
Paralytic Shellfish Poisoning ◽  
Shellfish Poisoning ◽  
Practical Applications ◽  
Drug Candidates ◽  
Shellfish Toxins ◽  
Paralytic Shellfish Toxins ◽  
Voltage Gated Sodium Channels ◽  
Paralytic Shellfish

Paralytic shellfish toxins (PSTs) are a group of toxins that cause paralytic shellfish poisoning through blockage of voltage-gated sodium channels. PSTs are produced by prokaryotic freshwater cyanobacteria and eukaryotic marine dinoflagellates. Proliferation of toxic algae species can lead to harmful algal blooms, during which seafood accumulate high levels of PSTs, posing a health threat to consumers. The existence of PST-transforming enzymes was first remarked due to the divergence of PST profiles and concentrations between contaminated bivalves and toxigenic organisms. Later, several enzymes involved in PST transformation, synthesis and elimination have been identified. The knowledge of PST-transforming enzymes is necessary for understanding the processes of toxin accumulation and depuration in mollusk bivalves. Furthermore, PST-transforming enzymes facilitate the obtainment of pure analogues of toxins as in natural sources they are present in a mixture. Pure compounds are of interest for the development of drug candidates and as analytical reference materials. PST-transforming enzymes can also be employed for the development of analytical tools for toxin detection. This review summarizes the PST-transforming enzymes identified so far in living organisms from bacteria to humans, with special emphasis on bivalves, cyanobacteria and dinoflagellates, and discusses enzymes’ biological functions and potential practical applications.

scholarly journals Dose-Response Modelling of Paralytic Shellfish Poisoning (PSP) in Humans

Toxins ◽  
2018 ◽  
Vol 10 (4) ◽  
pp. 141 ◽  
Author(s):  
Nathalie Arnich ◽  
Anne Thébault
Keyword(s):  
Epidemiological Data ◽  
Paralytic Shellfish Poisoning ◽  
Shellfish Poisoning ◽  
Marine Toxins ◽  
Paralytic Shellfish Toxins ◽  
Paralytic Shellfish ◽  
Adverse Effect Level ◽  
Effect Level ◽  
Human Poisoning ◽  
Response Modelling

Paralytic shellfish poisoning (PSP) is caused by a group of marine toxins with saxitoxin (STX) as the reference compound. Symptoms in humans after consumption of contaminated shellfish vary from slight neurological and gastrointestinal effects to fatal respiratory paralysis. A systematic review was conducted to identify reported cases of human poisoning associated with the ingestion of shellfish contaminated with paralytic shellfish toxins (PSTs). Raw data were collected from 143 exposed individuals (113 with symptoms, 30 without symptoms) from 13 studies. Exposure estimates were based on mouse bioassays except in one study. A significant relationship between exposure to PSTs and severity of symptoms was established by ordinal modelling. The critical minimal dose with a probability higher than 10% of showing symptoms is 0.37 µg STX eq./kg b.w. This means that 10% of the individuals exposed to this dose would have symptoms (without considering the severity of the symptoms). This dose is four-fold lower than the lowest-observed-adverse-effect-level (LOAEL) established by the European Food Safety Authority (EFSA, 2009) in the region of 1.5 μg STX eq./kg b.w. This work provides critical doses that could be used as point of departure to update the acute reference dose for STX. This is the first time a dose-symptoms model could be built for marine toxins using epidemiological data.

scholarly journals Accumulation and Elimination Dynamics of the Hydroxybenzoate Saxitoxin Analogues in Mussels Mytilus galloprovincialis Exposed to the Toxic Marine Dinoflagellate Gymnodinium catenatum

Toxins ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 428 ◽  
Author(s):  
Pedro Reis Costa ◽  
Ana Braga ◽  
Andrew Turner
Keyword(s):  
Mytilus Galloprovincialis ◽  
Paralytic Shellfish Poisoning ◽  
Shellfish Poisoning ◽  
Paralytic Shellfish Toxins ◽  
Algae Blooms ◽  
Food Borne ◽  
Paralytic Shellfish ◽  
Food Borne Illness ◽  
Marine Dinoflagellates ◽  
Gymnodinium Catenatum

Paralytic shellfish poisoning (PSP) is a severe food-borne illness, caused by the ingestion of seafood containing paralytic shellfish toxins (PST), which are naturally produced by marine dinoflagellates and accumulate in shellfish during algae blooms. Novel PST, designated as hydroxybenzoate analogues (also known as GC toxins), was relatively recently discovered in Gymnodinium catenatum strains worldwide. However, to date, there have been no studies examining their accumulation in shellfish. In this study, mussels (Mytilus galloprovincialis) were exposed to G. catenatum for five days and then exposed to a non-toxic diet for 24 h, to investigate the toxin’s accumulation/elimination dynamics. As determined by UHPLC-HILIC-MS/MS, the hydroxybenzoate analogues, GC1 to GC6, comprised 41% of the algae toxin profile and only 9% in mussels. Elimination of GC toxins after 24 h was not evident. This study highlights that a relevant fraction of PST in mussels are not routinely analysed in monitoring programs and that there is a need to better understand the toxicological potential of the hydroxybenzoate analogues, in order to properly address the risk of G. catenatum blooms.

Multiplexed ELISA screening assay for nine paralytic shellfish toxins in human plasma

The Analyst ◽  
2019 ◽  
Vol 144 (15) ◽  
pp. 4702-4707 ◽  
Author(s):  
Padmanabhan Eangoor ◽  
Amruta Sanjay Indapurkar ◽  
Mani Deepika Vakkalanka ◽  
Jennifer Sporty Knaack
Keyword(s):  
Human Plasma ◽  
Paralytic Shellfish Poisoning ◽  
Rapid Screening ◽  
Shellfish Poisoning ◽  
Screening Assay ◽  
Shellfish Toxins ◽  
Paralytic Shellfish Toxins ◽  
Paralytic Shellfish

Paralytic shellfish poisoning is a lethal syndrome that can develop in humans who consume shellfish contaminated with paralytic shellfish toxins. This rapid screening assay can be used to quickly diagnose exposure to paralytic shellfish toxins.

scholarly journals Parallel Analyses of Alexandrium catenella Cell Concentrations and Shellfish Toxicity in the Puget Sound

2010 ◽  
Vol 76 (14) ◽  
pp. 4647-4654 ◽  
Author(s):  
Sonya T. Dyhrman ◽  
Sheean T. Haley ◽  
Jerry A. Borchert ◽  
Bob Lona ◽  
Nicole Kollars ◽  
...  
Keyword(s):  
Puget Sound ◽  
Toxicity Testing ◽  
Paralytic Shellfish Poisoning ◽  
Economic Resources ◽  
Cell Distribution ◽  
Shellfish Poisoning ◽  
Alexandrium Catenella ◽  
Paralytic Shellfish Toxins ◽  
Paralytic Shellfish ◽  
Quantitative Pcr Assay

ABSTRACT Alexandrium catenella is widespread in western North America and produces a suite of potent neurotoxins that cause paralytic shellfish poisoning (PSP) in humans and have deleterious impacts on public health and economic resources. There are seasonal PSP-related closures of recreational and commercial shellfisheries in the Puget Sound, but the factors that influence cell distribution, abundance, and relationship to paralytic shellfish toxins (PSTs) in this system are poorly described. Here, a quantitative PCR assay was used to detect A. catenella cells in parallel with state shellfish toxicity testing during the 2006 bloom season at 41 sites from April through October. Over 500,000 A. catenella cells liter−1 were detected at several stations, with two main pulses of cells driving cell distribution, one in June and the other in August. PSTs over the closure limit of 80 μg of PST 100 per g of shellfish tissue were detected at 26 of the 41 sites. Comparison of cell numbers and PST data shows that shellfish toxicity is preceded by an increase in A. catenella cells in 71% of cases. However, cells were also observed in the absence of PSTs in shellfish, highlighting the complex relationship between A. catenella and the resulting shellfish toxicity. These data provide important information on the dynamics of A. catenella cells in the Puget Sound and are a first step toward assessing the utility of plankton monitoring to augment shellfish toxicity testing in this system.

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