Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Shellfish Poisoning”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 829 records · Page 46Linked to original sources

Neurologic illness associated with eating Florida pufferfish, 2002.

Since January 1, 2002, human illness after eating pufferfish caught in waters near Titusville, Florida, has been reported (Figure 1). The illnesses were manifested by neurologic symptoms consistent with exposure to paralytic shellfish toxins. Laboratory analysis in early April confirmed the presence of saxitoxin in uneaten pufferfish. This report presents selected case examples and summarizes all cases reported to the Toxic Exposure Surveillance System of the American Association of Poison Control Centers (TESS).

Adult↗

Domoic acid-induced neurodegeneration resulting in memory loss is mediated by Ca2+ overload and inhibition of Ca2+ + calmodulin-stimulated adenylate cyclase in rat brain (review).

Domoic acid is a shellfish toxin which produces neurodegeneration and CNS dysfunction, notably a loss of short-term memory. This toxin was found in blue mussels (Mytilus edulis) cultivated in river water in the east coast of Prince Edward Island in Canada and caused human poisoning. The toxin was localized in the stomach of blue mussels, which was engorged with algae, Nitzschia pungens, that were filtered from the surrounding water. The toxin was isolated from contaminated mussels or phytoplankton, and identified chemically as domoic acid (DOM) which is a tricarboxylic amino acid. Due to its structural resemblance to glutamic, aspartic and kainic acids, DOM was considered to produce excitotoxicity by similar mechanism(s). However, the latest evidence indicates differences in its mode of action from these excitatory agonists. We propose that DOM induces toxicity via changes in intracellular concentration of Ca2+ ([Ca2+]i). Results of our studies demonstrate that DOM elevated [Ca2+]i in brain slices. Glucose deprivation and removal of Na+ from the Krebs-bicarbonate medium further elevated [Ca2+]i, suggesting a relationship between glucose metabolism (cell energy), Na+ and Ca2+ transfer across neuronal membrane. DOM-induced rise in [Ca2+]i was due to enhanced Ca2+ influx and its mobilization from the endoplasmic reticulum. In addition, diminished Ca2+-ATPase activity due to lack of ATP, and variable amounts and expression of calcium binding proteins (CaBP) appear to contribute to an elevation in [Ca2+]i in response to DOM. Most interestingly, DOM inhibited Ca2+ and calmodulin-stimulated adenylate cyclase activity in brain membranes, resulting in reduced level of cyclic AMP. Cyclic AMP is known to activate protein kinase A to enhance phosphorylation of Ca2+ channels, thereby, reducing Ca2+ influx to prevent the development of Ca2+ overload which is detrimental to neuronal cell function (neuroprotection). However, DOM reduced cyclic AMP level, diminishing the feedback control of cyclic AMP on Ca2+ influx via Ca2+ channels, thereby, allowing continuing enhanced Ca2+ influx, resulting in Ca2+ overload which adversely affects many intracellular processes to induce toxicity. Ca2+ and CaM-stimulated adenylate cyclase activity in brain is highly correlated with the acquisition and retention of memory in different organisms. Calcium binding proteins bind Ca2+ reversibly and provide intracellular Ca2+ buffering, thereby, protecting neuronal cell from damage by Ca2+ overload in response to DOM. DOM appears to interfere with the cross talk between Ca2+ and cyclic AMP which is necessary for neuronal cell function. We have also demonstrated that DOM stimulates GLU release from synaptosomes and may produce some of its toxic effects via excess GLU in the neuronal synapse. In conclusion, DOM-induced neurodegeneration resulting in a loss of memory is mediated by Ca2+ overload, inhibition of Ca2+ and CaM-stimulated adenylate cyclase activity, and/or by the enhanced GLU release in rat brain.

Adenylyl Cyclases↗

Neurotoxic and molecular effects of methylmercury in humans.

Mercurials are global environmental pollutants deriving from natural processes and anthropogenic activities. Most human exposure to mercury occurs through the intake of fish, shellfish, and sea mammals contaminated with methylmercury. Methylmercury is bioaccumulated and biomagnified in the aquatic food chain and reaches its highest levels in top predatory fish. The neurotoxic hazard posed by methylmercury to humans and the unique susceptibility of the developing brain have been well documented following the mass poisonings occurring in Japan and Iraq. Adult cases of methylmercury poisoning are characterized by the delayed onset of symptoms and by the focal degeneration of neurons in selected brain regions (for example, cerebral cortex and cerebellum). Why the fetus displays different neuropathological effects and a higher sensitivity to methylmercury relative to the adult is still unknown. Depending on the degree of in utero exposure, methylmercury may result in effects ranging from fetal death to subtle neurodevelopmental delays. On the basis of epidemiological studies performed in populations having moderate chronic methylmercury exposure, no definitive consensus has been reached to date on the safety level of maternal exposure during pregnancy. Among the multiple mechanisms believed to contribute to methylmercury neurotoxicity, methylmercury-induced microtubule alterations, oxidative damage, impairment of calcium homeostasis, and the potentiation of glutamatergic neurotransmission are presented in this review.

Adult↗

Staphylococcal food poisoning in the United Kingdom, 1969-90.

Between 1969 and 1990 strains of Staphylococcus aureus from 359 outbreaks and sporadic cases of staphylococcal food poisoning in the United Kingdom were examined in the PHLS Food Hygiene Laboratory for the production of enterotoxin. In a number of instances the incriminated foods were also examined for the presence of enterotoxin. Strains from 79% of incidents produced enterotoxin A alone or together with another enterotoxin. The level of S. aureus present in the foods ranged from no viable S. aureus detected to 1.5 x 10(10) c.f.u./g with a median of 3.0 x 10(7) c.f.u./g. Enterotoxin was detected in foods in the absence of viable S. aureus in only two outbreaks and in both cheese was the implicated food. Meat, poultry or their products were the vehicle in 75% of incidents with ham and chicken most frequently implicated. Other foods included fish and shellfish (7%) and milk and milk products (8%). Most contamination took place in the home followed by restaurants and shops. Seventy-one percent of the incident strains were lysed by phages of group III or I/III.

Bacterial Toxins↗

Occurrence and sequestration of toxins in food chains.

Animals may acquire toxicity by absorbing toxic compounds from their food, e.g. from plants or other animals. Sequestration and accumulation of toxins may provide protection from predators, which learn to avoid this prey because of unpleasant experiences such as bitter taste. This is a common phenomenon in marine as well as in terrestrial ecosystems. Moreover, toxins may enter food chains where they accumulate reaching high, often lethal concentrations. Palytoxin which had been primarily detected in marine zoanthids (Palythoa sp.), occurs also in a wide range of other animals, e.g. in sponges, corals, shellfish, polychaetes and crustaceans, but also in fish, which feed on crustaceans and zoanthids as well. These animals exhibit a high resistance to the toxin's action. The mechanisms which protect the Na+, K+-ATPase of their cell membranes, the primary target of palytoxin, is unknown. Sequestration of the toxin by other animals may cause health problems due to food poisoning.

Acrylamides↗

High prevalence of thermostable direct hemolysin (TDH)-like toxin in Vibrio mimicus strains isolated from diarrhoeal patients.

A total of 17 isolates of Vibrio mimicus from patients, 29 from environment and 2 from food was examined for toxigenicity. Sixteen (94%) clinical isolates and one (50%) from food produced TDH-like toxin, whereas none of the environmental isolates did so. The food from which V. mimicus with TDH-like toxin production was isolated, was one which had caused food poisoning. Only one environmental strain produced CT-like toxin, whilst ST-like toxin was not detected from any strains tested.

Animals↗

Human poisoning by ingestion of a sea hare (Dolabella auricularia).

A case-report of poisoning by ingestion of a sea hare, which is thought to be the first report of human poisoning, is presented. The clinical signs were mainly neurological with tremor, psychomotor over-activity, ataxia and muscle twitching being predominant. It is suggested that organic bromine compounds are responsible for the effects.

Adult↗

The microbiology of cooked prawns and shrimps on retail sale.

In an inter-laboratory survey, 148 samples of cooked prawns and shrimps were obtained at the point of sale to the consumer. Salmonellae and Vibrio parahaemolyticus were not detected. Yersinia enterocolitica was isolated from three samples. Results for total viable count and presence of Escherichia coli and Staphylococcus aureus complied well with available guidelines for imported cooked prawns, suggesting that the risk of food poisoning from retail samples of these foods in the South of England is minimal.

Decapoda↗

Hair mercury levels of residents in China, Indonesia, and Japan.

The authors used gold-amalgamation cold-vapor atomic absorption spectrometry and ECD-gas chromatography to analyze total mercury and methylmercury levels in hair samples obtained from 362 residents in Harbin, China; Medan, Indonesia; and Tokushima, Japan. In this study, the authors initially questioned whether mercury levels in hair differed among different study areas, and if there were differences, they questioned the contributing factors. In the three countries surveyed, total mercury and methylmercury levels in hair were lowest in residents of China and were highest in residents of Japan. In the district of Tokushima, Japan, total mercury and methylmercury levels were highest in the coastal district, followed by the middle district; the lowest levels occurred in the mountainous district. In Japan, an individual's total mercury level correlated very closely with that person's methylmercury level; in China and Indonesia, the correlation between these 2 parameters was low. No subjects in China or Indonesia had high levels of methylmercury in hair; this was true even if their total mercury levels were high. This finding suggests that the high total mercury levels observed in some residents of China and Indonesia reflected exposure to inorganic mercury. In Japan, mercury (especially methylmercury) levels in hair samples were quite high. Fish and shellfish, caught in seas uncontaminated by human activity, appeared to be major sources of the high levels of hair mercury in Japanese subjects.

Adult↗

Cadmium in foods and the diet.

Information on the sources of cadmium in food are presented and the effects of raised environmental levels of cadmium on the concentration of cadmium in plant based foods, fish and shellfish, meat and offals, and dairy produce are discussed. Information is also presented on normal dietary intakes of cadmium and how these intakes may be elevated by environmental pollution or atypical dietary habits. The estimation of dietary intakes of cadmium using data about extreme intakes of specific foods is described.

Adult↗

[Characteristics of virulence gene in Vibrio parahaemolyticus strains isolated from clinical patients and environment in Hangzhou, China].

OBJECTIVES: To investigate the characteristics of virulence gene in Vibrio parahaemolyticus strains isolated from clinical patients and environment in Hangzhou, China. METHODS: Thermostable direct hemolysin gene (tdh) and thermostable direct hemolysin-related hemolysin gene (trh) were determined in a total of 174 strains of V. parahaemolyticus isolated from patients and environment (seafood) in Hangzhou area by PCR. RESULTS: The tdh was found in 92 out of 94 V. parahaemolyticus strains from food poisoning patients and in 33 out of 34 strains from sporadic diarrhea patients, and trh was not detected in all above clinical strains. Meanwhile the tdh was negative in all V. parahaemolyticus strains from environment, and the trh was also negative except one strain with urease activity. All strains with trh negative had no the activity of urease. CONCLUSIONS: The V. parahaemolyticus strains from food poisoning patients and sporadic diarrhea patients are tdh positive and trh negative. The V. parahaemolyticus strains with tdh negative and almost trh positive in environment might be a potential pathogen in Hangzhou.

Bacterial Proteins↗

Occurrence of saxitoxin in puffer fish.

Three species of puffer fish, Takifugu poecilonotus, T. vermicularis and T. radiatus, were examined for the presence of toxic components other than tetrodotoxin. Saxitoxin, a paralytic shellfish toxin, was found in the livers, ovaries and digestive tracts of the first two species but not in the last species. The puffers are assumed to accumulate saxitoxin by feeding on bivalves that have ingested a toxic dinoflagellate Protogonyaulax tamarensis. Another toxic component is present in the liver of T. poecilonotus, but its structural relationship to tetrodotoxin or saxitoxin is questionable.

Animals↗