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Paralytic shellfish toxins (PSTs) are widely distributed in shellfish along the coast of China, causing a serious threat to consumer health; however, there is still a lack of large-scale systematic investigations and risk assessments. Herein, 641 shellfish samples were collected from March to November 2020, and the PSTs’ toxicity was detected via liquid chromatography–tandem mass spectrometry. Furthermore, the contamination status and potential dietary risks of PSTs were discussed. PSTs were detected in 241 shellfish samples with a detection rate of 37.60%. The average PST toxicities in mussels and ark shells were considerably higher than those in other shellfish. The PSTs mainly included N-sulfonylcarbamoyl toxins (class C) and carbamoyl toxins (class GTX), and the highest PST toxicity was 546.09 μg STX eq. kg−1. The PST toxicity in spring was significantly higher than those in summer and autumn (p < 0.05). Hebei Province had the highest average PST toxicity in spring. An acute exposure assessment showed that consumers in Hebei Province had a higher dietary risk, with mussels posing a significantly higher dietary risk to consumers. This research provides reference for the green and sustainable development of the shellfish industry and the establishment of a shellfish toxin prevention and control system.

BackgroundFatal cases of exposure to paralytic shellfish toxins and palytoxins have occurred in companion animals but are poorly described.MethodsWe describe one case of paralytic shellfish poisoning (PSP) and three cases of palytoxin poisoning in dogs.ResultsMild PSP occurred following ingestion of crab while walking on a beach. Analysis confirmed the presence of paralytic shellfish toxins, particularly decarbamoyl saxitoxin, in clinical samples and marine organisms. This case occurred shortly after an outbreak of PSP in dogs on the eastern coast of England. Palytoxin poisoning occurred in a dog after it chewed coral removed from an aquarium. Signs included collapse, hypothermia, bloody diarrhoea and respiratory distress. The dog was euthanised due to rapid deterioration and poor prognosis. Palytoxin was not detected in a premortem blood sample. Two other dogs in a separate incident developed only mild signs (fever and respiratory distress) after suspected exposure to aerosolised palytoxin and recovered within a few hours.ConclusionCases of PSP are episodic and not common in dogs. Cases of palytoxin exposure are reportedly increasing in humans, and there is presumably also an increased risk to pets. There is no specific treatment for PSP or palytoxin poisoning.

Domoic acid epileptic disease is characterized by spontaneous recurrent seizures weeks to months after domoic acid exposure. The potential for this disease was first recognized in a human case study of temporal lobe epilepsy after the 1987 amnesic shellfish-poisoning event in Quebec, and was characterized as a chronic epileptic syndrome in California sea lions through investigation of a series of domoic acid poisoning cases between 1998 and 2006. The sea lion study provided a breadth of insight into clinical presentations, unusual behaviors, brain pathology, and epidemiology. A rat model that replicates key observations of the chronic epileptic syndrome in sea lions has been applied to identify the progression of the epileptic disease state, its relationship to behavioral manifestations, and to define the neural systems involved in these behavioral disorders. Here, we present the concept of domoic acid epileptic disease as a delayed manifestation of domoic acid poisoning and review the state of knowledge for this disease state in affected humans and sea lions. We discuss causative mechanisms and neural underpinnings of disease maturation revealed by the rat model to present the concept for olfactory origin of an epileptic disease; triggered in dendodendritic synapases of the olfactory bulb and maturing in the olfactory cortex. We conclude with updated information on populations at risk, medical diagnosis, treatment, and prognosis.

This investigation was undertaken in response to an outbreak of suspected shellfish poisoning in Zhejiang Province, China. The objectives of this project were to confirm the outbreak and to identify the aetiology, source and mode of transmission. A probable case was defined as an individual with diarrhea (≥3 times/day) plus at least one of the following symptoms: fever (≥37.5°C), vomiting, or abdominal pain after consuming seafood between May 23(rd) and May 28(th), 2011. Using a case-control study design, we compared exposures to suspected seafood items and cooking methods between 61 probable cases and 61 controls. Over 220 suspected or probable cases of diarrhetic shellfish poisoning (DSP) were identified (incidence of 18 cases per 100,000). The case control study revealed that 100% of cases and 18% of controls had eaten mussels during the exposure period (OR = ∞, χ(2) = 84.72,P = 0.000). The number of mussels consumed was related to DSP risk (P = 0.004, χ2 test for trend). Consumption of other seafood items was not associated with disease. The frequency of diarrhea and vomiting were positively correlated with the number of mussels consumed (r = 0.424 and r = 0.562, respectively). The frequency of vomiting and the incubation period were significantly correlated with the total time the mussels were boiled (r = 0.594 and r = -0.336, respectively). Mussels from 3 food markets and one family contained Okadaic acid (OA) and Dinophysistoxin-1 (DTX-1). This outbreak was attributed to the consumption of mussels contaminated by DSP-toxins (OA and DTX-1) which are produced by different species of dinoflagellates (toxic microalgae) from the genus Dinophysis or Prorocentrum. Suspension of mussel sales and early public announcements were highly effective in controlling the outbreak, although oversight of seafood quality should be a priority to prevent future contamination and outbreaks.

The paralytic shellfish poisoning toxins (PSTs) were, as their name suggests, discovered as a result of human poisoning after consumption of contaminated shellfish. More recently, however, the same toxins have been found to be produced by freshwater cyanobacteria. These organisms have worldwide distribution and are common in our sources of drinking water, thus presenting another route of potential human exposure. However, the regulatory limits for PSTs in drinking water are considerably lower than in shellfish. This has increased the need to find alternatives to the mouse bioassay, which, apart from being ethically questionable, does not have a limit of detection capable of detecting the PSTs in water at the regulated concentrations. Additionally, the number of naturally occurring PSTs has grown substantially since saxitoxin was first characterised, markedly increasing the analytical challenge of this group of compounds. This paper summarises the development of chromatographic, toxicity, and molecular sensor binding methodologies for detection of the PSTs in shellfish, cyanobacteria, and water contaminated by these toxins. It then summarises the advantages and disadvantages of their use for particular applications. Finally it recommends some future requirements that will contribute to their improvement for these applications.

From June 2006 to January 2007 passive samplers (solid phase adsorbing toxin tracking, SPATT) were tested as a monitoring tool with weekly monitoring of phytoplankton and toxin content (liquid chromatography–mass spectrometry, LC-MS) in picked cells of Dinophysis and plankton concentrates. Successive blooms of Dinophysis acuminata, D. acuta and D. caudata in 2006 caused a long mussel harvesting closure (4.5 months) in the Galician Rías (NW Spain) and a record (up to 9246 ng·g resin-week−1) accumulation of toxins in SPATT discs. Best fit of a toxin accumulation model was between toxin accumulation in SPATT and the product of cell densities by a constant value, for each species of Dinophysis, of toxin content (average) in picked cells. Detection of Dinophysis populations provided earlier warning of oncoming diarrhetic shellfish poisoning (DSP) outbreaks than the SPATT, which at times overestimated the expected toxin levels in shellfish because: (i) SPATT accumulated toxins did not include biotransformation and depuration loss terms and (ii) accumulation of toxins not available to mussels continued for weeks after Dinophysis cells were undetectable and mussels were toxin-free. SPATT may be a valuable environmental monitoring and research tool for toxin dynamics, in particular in areas with no aquaculture, but does not provide a practical gain for early warning of DSP outbreaks.

The illness of three people due to diarrhetic shellfish poisoning (DSP) following their ingestion of recreationally harvested mussels from Sequim Bay State Park in the summer of 2011, resulted in intensified monitoring for diarrhetic shellfish toxins (DSTs) in Washington State. Rapid testing at remote sites was proposed as a means to provide early warning of DST events in order to protect human health and allow growers to test “pre-harvest” shellfish samples, thereby preventing harvest of toxic product that would later be destroyed or recalled. Tissue homogenates from several shellfish species collected from two sites in Sequim Bay, WA in the summer 2012, as well as other sites throughout Puget Sound, were analyzed using three rapid screening methods: a lateral flow antibody-based test strip (Jellett Rapid Test), an enzyme-linked immunosorbent assay (ELISA) and a protein phosphatase 2A inhibition assay (PP2A). The results were compared to the standard regulatory method of liquid chromatography coupled with tandem mass spectroscopy (LC-MS/MS). The Jellett Rapid Test for DSP gave an unacceptable number of false negatives due to incomplete extraction of DSTs using the manufacturer’s recommended method while the ELISA antibody had low cross-reactivity with dinophysistoxin-1, the major toxin isomer in shellfish from the region. The PP2A test showed the greatest promise as a screening tool for Washington State shellfish harvesters.

Matrix reference materials are an essential component for the validation and quality control of analytical methodologies for the quantitation of marine biotoxins in shellfish. Given the potential advantages of reference materials in powder form, a study was conducted to assess the feasibility for the production of a freeze-dried oyster tissue reference material containing a range of important paralytic shellfish poisoning toxins. One bulk sample of a wet oyster tissue homogenate was generated following mass culturing of toxic Alexandrium and oyster feeding experiments. The bulk tissue was used to prepare untreated wet frozen aliquots with the remainder being freeze-dried and processed into appropriately-sized powder samples. A pre-column oxidation LC-FLD analysis was used to confirm the absence of any chromatographic artefacts resulting from the processing and to confirm acceptable homogeneity of the tissues. Excellent stability over both the short-term (1 month) and long-term (1 year) of the freeze-dried material was demonstrated as compared with the stability of the untreated wet tissue. A post-column oxidation LC-FLD method was used to confirm the absence of toxin epimerisation in freeze-dried tissues which were observed in the wet tissues. Overall the work showed the feasibility of an approach to produce a homogenous freeze-dried oyster matrix material with enhanced stability in comparison to the untreated wet tissue. The potential for use of the process for preparation of large scale production batches of a freeze-dried CRM for paralytic shellfish poisoning toxins has therefore been demonstrated.

Bivalve shellfish samples containing paralytic shellfish poisoning toxins were subjected to gamma irradiation dosage trials in order to assess the potential suitability of the technique in the production of toxin reference materials. Two candidate reference materials of tissue homogenates, mussels ( Mytilus sp.) and native oysters ( Ostrea edulis ), were prepared in-house. Both were subjected to gamma irradiation at four different dose levels, 3.0, 6.0, 13.0 and 18.1 kGy. Bacterial levels were shown to be eliminated in the mussels and significantly reduced in the oysters following irradiation at all four dose levels. Paralytic shellfish poisoning (PSP) toxin concentrations were not significantly reduced in any of the samples indicating the treatment had no adverse affect on the initial stability of any of the PSP toxins monitored. Chromatographic results showed near-identical profiles for treated and non-treated samples inferring that no fluorescent toxin degradation products or matrix interferences were produced during the irradiation process. Results therefore proved that gamma irradiation treatment reduced bacterial levels within paralytic shellfish poisoning reference materials without compromising analyte content, with the subsequent potential to enhance the stability of future candidate reference materials treated in this manner. Fig. 1 Cefas tubular bag photobioreactor used for mass culture of Alexandrium

The possible causative agent and shrimp species involved in a bait shrimp poisoning case that occurred in northern Taiwan was determined. Because the patient's symptoms were similar to those caused by boric acid and slightly similar to those caused by sulfite, the concentrations of boric acid and sulfite (as sulfur dioxide) in the patient's vomitus and in shrimp collected from bait stores and markets were analyzed. The concentration of boric acid was 36.8 to 37.1 mg/g in the patient's vomitus, 1.4 to 3.8 mg/g in shrimp meats obtained from bait stores, and not detectable (less than 0.001 mg/g) in shrimp meat obtained from commercial markets. No significant differences in sulfur dioxide concentrations (0.067 to 0.088 mg/g) were found in patient's vomitus and the shrimp meat from both bait stores and commercial markets. A fragment of the cytochrome b gene (∼406 bp) was amplified by PCR using a pair of primers (UCYTB151F and UCYTB270R) from shrimp meat of two species and the vomitus. The vomited shrimp was identified as Parapenaeus fissuroides on the basis of gene sequencing and restriction fragment length polymorphism patterns after treatment with endonuclease Alu I. Based on the patient's symptoms and analytical data, we concluded that boric acid at toxic levels had been illegally added to the bait shrimp P. fissuroides.