Paralytic shellfish poisoning contamination status and dietary exposure assessment in coastal cities of China / 预防医学

@#Paralytic shellfish poisoning contamination is a threat to human health. Based on review of research articles pertaining to paralytic shellfish poisoning contamination in shellfishes and assessment of dietary exposure to paralytic shellfish poisoning in coastal cities of China from 2007 to 2022, the article describes the status of paralytic shellfish poisoning contamination, influencing factors and dietary exposure assessment in different sea areas of China (Bohai Sea, Huanghai Sea, East China Sea and South China Sea), and the relatively high-level contamination of paralytic shellfish poisoning in shellfishes is found to strongly correlate with red tides caused by season and water temperature in the Bohai Sea and South China Sea areas. Acute exposure assessment based on point estimate model is commonly used for assessment of dietary exposure to paralytic shellfish poisoning, and the risk of human dietary exposure to paralytic shellfish poisoning is within the acceptable range in most areas. Intensified monitoring of paralytic shellfish poisoning contamination in shellfishes and full consideration of parameters like processing factor during dietary exposure assessment are required in the future to allow more precise results.

Bacterial community associated with Pyrodinium bahamense var. compressum during late exponential growth phase based on 16S rRNA gene sequence analysis

Aims@#Pyrodinium bahamense var. compressum is one of the principal causal agents of harmful algal blooms (HABs) in the coastal waters of Sabah, Malaysia. Seafood and aquaculture products tainted with lethal concentrations of the principal neurotoxin, saxitoxin, have been implicated in mortality and morbidity. The bacteria-algae association may play a key role in paralytic shellfish toxin (PST) production during a toxic bloom event. The production of PST during a harmful bloom is unclear and research on the bacterial diversity associated with Sabah P. bahamense is scarce. The present study examined the cultivable bacteria diversity associated with P. bahamense through 16S ribosomal RNA (rRNA) gene sequence analysis.@*Methodology and results@#The V3-V4 region of the 16S rRNA gene sequence was amplified and used to identify bacterial populations associated with P. bahamense var. compressum. A total of 62 isolates were successfully isolated, belonging to three different phyla, which were Proteobacteria; 55 (89%), Bacteroidetes; 6 (10%) and Actinobacteria; 1 (1%). Out of 55 Proteobacteria, 27 isolates were gamma-Proteobacteria (Marinobacter salsuginis) and 28 of the isolates were alpha-Proteobacteria; Mameliella atlantica (13), Roseibium denhamense (10) and Roseibium hamelinense (5). The remaining bacteria isolates from the phyla Bacteroidetes and Actinobacteria were identified as Muricauda lutimaris (6) and Micrococcus luteus (1), respectively.@*Conclusion, significance and impact of study@#The analysis of the bacterial 16S rRNA gene revealed multiple bacterial taxa associated with the toxic P. bahamense var. compressum bloom. The findings of the present work will pave the way for further studies aimed at isolating and characterizing genes involved in the saxitoxin biosynthesis in the associated bacteria.

Toxinas Algales en el Mar Argentino: nuevos hallazgos, nuevos desafíos / Algal Toxins in the Argentine Sea: new findings, new challenges

Resumen Las floraciones de algas nocivas son un problema cada vez más frecuente a nivel mundial que ocasiona severos daños sobre la salud pública, pérdidas económicas en acuicultura, perjuicios al turismo y episodios de mortalidad de poblaciones naturales de peces, aves y mamíferos marinos. Las toxinas son producidas por el fitoplancton y se acumulan en moluscos bivalvos que se alimentan por filtración del agua siendo estos los principales vectores de intoxicación humana. En el Mar Argentino, se han reportado toxinas marinas de origen microalgal asociadas con cuatro síndromes de intoxicación por moluscos. Los síndromes más graves por su extensión, frecuencia, toxicidad y organismos afectados, son los originados por el dinoflagelado Alexandrium cate-nella responsable de la Intoxicación Paralizante por Moluscos la cual ha ocasionado numerosas muertes humanas. Seguidamente, la más leve, en cuanto a gravedad y frecuencia, ha sido la Intoxicación Diarreica por Moluscos. En contraste, el ácido domoico, conocido como toxina amnésica de moluscos, no ha producido hasta ahora intoxicaciones humanas. Recientemente, se amplió el rango de toxinas para la región al registrarse las toxinas y los dinoflagelados productores de la Intoxicación Azaspirácidos por Moluscos. Además, se han detectado las potencialmente tóxicas Yessotoxinas y Espirolidos, cuyos mecanismos de acción y toxicidad están siendo aún evaluados a nivel mundial. Estas toxinas emergentes para la región, representan un riesgo potencial para la salud e inconvenientes socioeconómicos por el cierre de los sitios de explotación de moluscos. Ciertamente presentan un nuevo desafío, pues la detección y cuantificación sólo puede realizarse por medio de métodos basados en HPLC - espectrometría de masas, lo cual dificulta el monitoreo en laboratorios regionales en el país. La herramienta clave de manejo es la prevención, a través de políticas, regulaciones y sistemas de monitoreo y control de cada grupo de toxinas. A través de estas mejoras, se anticipa que no sólo disminuirá el número de afectados por estas intoxicaciones, si no que se podrán realizar vedas más eficientes, asegurando un equilibrio que proteja tanto la salud pública como el desarrollo de la industria pesquera.

Abstract Harmful algal blooms are an increasingly common problem worldwide, causing severe damage to public health, economic losses in aquaculture, damage to tourism and mortality events of natural populations of fish, birds and marine mammals. The toxins are produced by phytoplankton and accumulated in bivalve molluscs that feed on water filtration, being these main vectors of human intoxication. In the Argentine Sea marine toxins of microalgal origin have been reported associated with four shellfish poisoning syn-dromes. The most serious due to their extension, frequency, toxicity and affected organisms are those caused by the dinoflagellate Alexandrium catenella responsible for the Paralytic shellfish poisoning that has caused numerous human deaths. Then, the mildest, in severity and frequency, is the Diarrhetic shellfish poisoning. In contrast, domoic acid, known as Amnesic shellfish toxin, has not produced human intoxications yet. Recently, toxins and dinoflagellate species causing Azaspiracid shellfish poisoning have been re-corded, expanding the range of toxins for the region. In addition, the potentially toxic Yessotoxins and Spirolides have been detected, whose mechanism of action and toxicity is still being evaluated worldwide. These emerging toxins represent a potential risk to public health and socioeconomic activities due to the eventual closure of mollusc exploitation sites. They certainly present a new challenge, since detection and quantification can only be carried out using methods based on HPLC - mass spectrometry, which makes monitor-ing in regional laboratories difficult. Prevention through policies, regulations, and monitoring and control systems of each toxin group is the key management tool. These preventive measures are expected to contribute to reducing the number of poisonings and to ap-plying more efficient fisheries closures, ensuring a balance that protects both public health and the development of the fishing industry.

Determination of PSP Toxins in Moroccan Shellfish by MBA, HPLC and RBA Methods: Links to Causative Phytoplankton Alexandrium minutum

Paralytic shellfish poisoning (PSP) toxins are secondary metabolites of the toxic species of phytoplankton. The consumption of shellfish accumulating these toxins can cause neurological symptoms and even death. Within the framework of the surveillance program of seafood safety along the Moroccan littoral environment established by National Institute of Fisheries Research (INRH), a study of PST was conducted from 2004 to 2016 in south Moroccan’s shellfish, mussels from south Agadir region and Razor Shell from Dakhla bay. The surveillance was carried out bi-monthly or weekly using the AOAC official method of analysis (AOAC 959.08) mouse bioassay (MBA). In parallel, monitoring of toxic phytoplankton in water was conducted. With the aim to determine the shellfish toxin profile, ion-pair high-performance liquid chromatography with post-column derivatisation and fluorescence detection (HPLC-FD) was performed. The Receptor Binding Assay (RBA) also was used for determination of total toxicity of PSP toxins in Agadir’s mussels.In both regions, the analysis of seawater revealed the presence of the toxic algae Alexandrium spp during toxics events. Along the coast of Agadir, PSP toxins in shellfish were associated with the presence of Alexandrium cf. minutum in seawater. These toxic events were widely distributed in time and space and mainly detected during the summer and fall seasons. In some samples concentrations exceeded the sanitary threshold (ST) of 800 ?g eq STX /kg. HPLC analysis revealed that Saxitoxin and Gonyautoxins dominated the toxin profile. The comparison between different methods showed a strong uphill (positive) linear relationship, with a coefficient correlation of r=0.79 between MBA and HPLC and r = 0.809 between MBA and RBA

Florecimientos algales nocivos producidos por Pyrodinium bahamense en Oaxaca, México (2009-2010) / Harmful algal blooms produced by Pyrodinium bahamense in Oaxaca, Mexico (2009-2010)

Objetivo. Monitorear el dinoflagelado Pyrodinium bahamense y sus toxinas en ostión de roca Striostrea prismatica en Santiago Astata y en Puerto Escondido, Oaxaca, de septiembre de 2009 a junio de 2010. Material y métodos. Se analizó mensualmente la abundancia de Pyrodinium bahamense mediante el método de Sedgewick-Rafter y la concentración de toxinas paralizantes y perfil tóxico en tejido blando del molusco en muestras compuestas de cada zona por el método de cromatografía líquida de alta resolución. Resultados. Se encontró alta abundancia de Pyrodinium bahamense en Santiago Astata en diciembre, febrero, abril y junio, y en Puerto Escondido en abril y junio. Los niveles de toxinas paralizantes fueron superiores al límite permisible para consumo humano en Santiago Astata en noviembre, diciembre, enero, febrero y junio; en la zona de Puerto Escondido, en diciembre y junio. Conclusiones. Estos niveles de toxinas representaron riesgo para la salud pública en la zona de estudio.

Objective. Pyrodinium bahamense monitoring in water and their toxins in rock oyster Striostrea prismatica in Santiago Astata and Puerto Escondido Oaxaca was performed from September 2009 to July 2010. Materials and methods. Pyrodinium bahamense abundance in water, and concentration and toxic profile of paralytic shellfish toxins were analyzed monthly in soft tissue of mollusk in composite samples in high performance liquid chromatography. Results. High abundance of Pyrodinium bahamense was found in Santiago Astata on December, February, April and June; and in Puerto Escondido on April and June. The concentrations of the paralyzing toxin that exceeded the regulatory limit for human consumption of mollusks (800 µg STX eq. kg-1) were presented in Santiago Astata on November, December, January, February and June; and in Puerto Escondido on December and June. Conclusions. For several months there was risk to public health due to the presence of paralytic shellfish toxins above the regulatory limit in oysters from the study area.

Development of an ICR mouse bioassay for toxicity evaluation in neurotoxic poisoning toxins-contaminated shellfish / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To develop an ICR (female) mouse bioassay (MBA) for toxicity confirmation and evaluation of neurotoxins (brevetoxins)-contaminated shellfish.</p><p><b>METHODS</b>Brevetoxins (BTX-B) as a causative agent of neurotoxic shellfish poisoning (NSP) under different shellfish matrices were intraperitoneally injected at different doses into mice to study their toxic effects and to differentiate the range of lethal and sublethal dosages. Their sensitivity and specificity were analyzed with 2 competitive ELISA kits for quantitative determination of standard BTX-B and dihydroBTX-B under different shellfish matrix-diluent combinations. Detection rates of MBA and two antibody-based assays for BTX-B from field NSP-positive shellfish samples were compared.</p><p><b>RESULTS</b>BTX-B could be detected in shellfish tissues at concentration of 50-400 μg/100 g under shellfish matrix-Tween-saline media, which were appropriate to identify toxic shellfish at or above the regulatory limit (80 μg/100 g shellfish tissues). The LD50 identified was 455 mg/kg for BTX-B under general shellfish matrices (excluding oyster matrices) dissolved in Tween-saline. The presence of shellfish matrices, of oyster matrices in particular, retarded the occurrence of death and toxicity presentation in mice. Two antibody-based assays, even in the presence of different shellfish matrix-diluent combinations, showed acceptable results in quantifying BTX-B and dihydroBTX-B well below the regulatory limit.</p><p><b>CONCLUSION</b>The two ELISA analyses agree favorably (correlation coefficient, r³⋝0.96; Student's t-tests, P>0.05) with the developed bioassay.</p>

Detection of shellfish toxins from scallops in Guangzhou seafood market

To evaluate scallop safety in the Guangzhou seafood market, contents of shellfish toxins in adductor muscle, mantle skirts, gills and visceral mass of scallops were examined using enzyme-linked immunosorbent assay (ELISA) and mouse unit assay. The results showed that: paralytic shellfish poisoning contents were up to 37.44 µg/100 g by ELISA and 319.99 MU/100 g by mouse unit assay, which did not exceed the limits of national standards (80 µg/100g and 400 MU/100 g); the contents of diarrhetic shellfish poisoning were 142.04 µg/100g and 0.2 MU/100 g, which exceeded the national standard limits (60 µg/100g); neurotoxic shellfish poisoning was undetectable; the contents of amnesic shellfish poisoning reached 220.12 µg/100g (no limit value could be referred to) . In addition, these poisons were present mainly in visceral mass and gills rather than adductor muscle and mantle skirts, suggesting that these toxins accumulate in a tissue-specific manner.(AU)

Detecção de ácido ocadaico em cultivo de mexilhões Perna perna, Angra dos Reis, RJ / Okadaic acid detection in mussel cultivation Perna perna, Angra dos Reis, RJ

A ficotoxina ácido ocadaico (AO) é produzida por um grupo de microalgas conhecidas como dinoflagelados. Os mexilhões, ao se alimentarem dessas microalgas, acumulam a toxina em sua glândula digestiva, desencadeando a Síndrome ou Envenenamento Diarreico por Moluscos (EDM) no ser humano. Os sintomas se apresentam em torno de 30 minutos após o consumo do molusco contaminado, variando entre náuseas, dores abdominais, vômitos e diarreia. Quando a ingestão da toxina acontece em quantidades inferiores a 48µg g-1, os sintomas não se desenvolvem, porém seu consumo continuado favorece o surgimento de tumores no trato gastrointestinal em razão do poder carcinogênico do AO. Este estudo pretendeu detectar e quantificar a toxina diarreica AO em mexilhões Perna perna coletados entre os meses de maio e outubro de 2006. A detecção do AO nos mexilhões foi realizada por Cromatografia Líquida de Alta Eficiência com Detecção Fluorimétrica (CLAE-DF). Os resultados cromatográficos indicaram a presença da toxina AO em baixas concentrações, em todas as amostras de mexilhões obtidas de maio a outubro de 2006. Os resultados indicam a necessidade da elaboração e aplicação efetiva de um programa de controle higiênico-sanitário dos moluscos, assim como o monitoramento do ambiente aquático, objetivando, acima de tudo, a segurança da saúde pública.

Okadaic acid (OA) is a phycotoxin produced by a group of microalgae known as Dino-flagellates. When mussels feed themselves from this micro seaweed the toxin accumulates in their hepatopancreas, triggering the Syndrome or Diarrhetic Shellfish Poisoning (DSP) in the human being. The symptoms appear around 30 minutes after the consumption of contaminated mussels and include abdominal nauseas, pains, vomits and diarrhea. When the toxin ingestion happens in amounts lower than 48µg g-1, the above described symptoms do not develop. However, the continued consumption favors the emergence of tumors in the gastrointestinal tract because of the high carcinogenic power of OA. This study aimed to detect and quantify the diarrheic toxin OA in Perna perna mussels collected between May and October 2006. The detection of OA in the mussels was carried out through High Performance Liquid Chromatography with Fluorimetric Detection (HPLC-FD). The chromatographic results indicate the presence of OA toxin in low concentrations in all the mussel samples gathered from May until October 2006. The results suggest the necessity of elaboration and effective application of a hygienic-sanitary mussel control program as well as environment monitoring, with the main aim of enhancing public health safety.

Paralytic Shellfish Poisoning by Saxitoxin: Two case reports

Paralytic shellfish poisoning results from consumption of mollusks that have fed on dinoflagellates capable of producing neurotoxins such as saxitoxin. The saxitoxin is concentrated in the shellfish and acts by decreasing sodium-channel permeability, thereby blocking neuronal transmission in skeletal muscles. Symptoms including paresthesia, perioral numbness, perioral tingling, nausea, vomiting, extremity numbness, extremity tingling, dizziness, ataxia, dysphagia, and weakness have been reported. In serious cases, respiratory hold may occur up to 6~24 hours after ingestion. Generally, the treatment for paralytic shellfish poisoning is supportive care, but mechanical ventilation is needed in serious cases acompanied by respiratory hold. We experienced two cases of paralytic shellfish poisoning. Respiratory hold was presented in one case and only mild paresthesia in the other case. After supportive management, including mechanical ventilation in former case, both patients were discharged without sequalae.

Toxicity of long-term intake of PSP at low level from shellfish on rats / 中国病理生理杂志

AIM: In order to investigate the possible cumulative and chronic toxicity of paralytic shellfish poisoning (PSP) and provide more information on toxicity of PSP. METHODS: The sub-acute toxicity of PSP was evaluated in the rat. PSP was extracted from the seafood in market, and the toxicity of the extract was determined by mouse bioassay. The extracts in different toxicity were administrated to rats through gastrotube for 35 days. The biochemical and pathological changes in vital tissues in rats were examined by the detections of some function indexes in blood and urine and the observations under optical microscope during both the exposure period and the subsequent 10-day withdrawal term. RESULTS: No biochemical and pathological changes in tissues occurred for the control and low-dose group (4.6 ?g STX/kg), whereas some changes happened for the middle (9.2 ?g STX/kg) and high groups (18.4 ?g STX/kg). In experiment, some renal function indexes changed in the mid-dose group, and some of the cardiac, hepatic and renal functions indexes altered for the high dose group with some changes in weight of the thymus gland and spleen. What is more, the liver and kidney became indistinct with some inflammatory changes, and some muscles had ruptured for the 40% rats in high-dose group. CONCLUSION: These results suggest that long-term intake of PSP at a concentration, which doesn't exceed the threshold of standard, has some toxicity on rats, and that the toxicity of PSP has an accumulative effect. In a word, it is unsafe for us to eat frequently bivalve seafood polluted by PSP toxins.

All about red tide and paralytic shellfish poisoning

In summary, we are presented with a patient who ingested mussel that are suspected to contain toxins that cause paralytic shellfish poisoning or PSP. Upon reaching the stomach, the digestive process accelerates the release of PSP toxins. The toxins are rapidly absorbed in the stomachs acidic medium and starts to work on the cellular Na channels, blocking the movement of Naions thus preventing the progression of the action potential with the absence of the action potential, there is a continued state of depolarization. This explains the feeling of numbness of the lips and fingertips, as seen in our patient, since these are the areas where nerve endings abound, and thus, are the areas most sensitive to these chemical changes. Our patient experienced this whole gamut of neurologic manifestations. He also started experiencing gastrointestinal symptoms such as epigastric pain and vomiting which are initially erroneously diagnosed as a separate problem Hearing hearsay reports on coconut milk being used as antidote for cases like these, the patient tried it too. The coconut milk, being an alkaline substance, must have stabilized some of the toxins, thus explaining the mild relief experienced by the patient prior to hospitalization. Upon reaching the hospitals, NGT was inserted and NaHCO3 lavage was done which further stabilized the toxins that were not yet absorbed, while those that were absorbed were excreted through the kidneys with the help of mannitol. After all these measures, the patient experienced considerable relief of the neurologic symptoms, though still with the intermitent epigastric pain erroneously diagnosed as Acid Peptic Disease and treated with antacids. Improvement of the neurologic complaints eventually lead to the discharge of the patient Our patient is just one of the lucky ones who benefited from immediate medical intervention to save his life. Many others arent so lucky - - - most of them never even know what hit them and thus could only look heavenwards hoping for divine intervention. Others are left to languish in understaffed overcrowded hospitals in far-flung places. Worse, a lot of those who have died of PSP never even get to a hospital Grim scenarios such as these are bound to occur yearly as long as pollution, deforestation, ignorance, and poverty prevail. We physician may not be able to curb these ills of society but we can certainly help, first and foremost by initiating the more crucial preventive measures, then by administering immediate and knowledgeable modes of treatment, and finally, by never losing the family physicians most important therapeutic tool: genuine concern for the patient. Hopefully, in doing so, we family physicians can join the family of man down to the sunset of our lives, enjoying Manila Bay for its red beautiful scape, and not for its red deadly tide.

Preliminary Research on the Methods of Fragmentation of the Cell Wall and the Toxicity of Alexandrium tamarense in Different Growth Phases / 环境与健康杂志

ve To study the growth curve of Alexandrium tamarense and the toxicity of paralytic shelfish poisoning(PSP) selected in different growth phases, as well as to quantitatively analyze the toxins and compare the different efficiency of breaking cell wall and their virtues and defects between freezing-thawing method and supersonic method, and to provide theoretical basis for the selection of the methods for extraction of PSP. Methods Cells were collected by suction filter, cell wall was broken by freezing-thawing method and supersonic method, the toxicities of Alexandrium tamarense among different growth phases were detected and compared. Results The growth of Alexandrium tamarense typically showed three phases which included a lag phase(0~9 days), an exponential growth phase(10~18 days), and a stationary phase(19~22 days) . The maximum toxicity of cells in the stationary phase appeared, especially in day 21 when the population of cells reached to 9.43?10-6 MU/cell, although the cells in the exponential phase grew fastest. Toxicity of the cells in the lag phase broken by freezing-thawing method was more stronger than that by supersonic method, that meant the toxicity of cells was lowered after the supersonic treatment. In additional, the filtering method for collecting cells presented a lower recovery rate of average 69.0% . Conclusion As for the comparing of freezing-thawing method and supersonic method, it was found that, when cells were in the same phase, the supersonic method had remarkable advantages, but it also had the disadvantage of lowering the tox-icity of cells. When in the same condition of growth and method of fragmentation, cells in the lag phase were broken most easily, and cells in the stationary phase were more difficult to be broken than those in the other two phases. Toxicity of cells was larger and larger with the time of incubation. The toxicity of cells in the lag phase had reached a higher intensity, although toxicities of cells in the next two phases would increase a little.