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Shellfish disease

Education, simple rules of personal hygiene and safe food preparation can prevent many diarrheal diseases. Hand washing with soap is an effective step in preventing spread of illness. Human feces must always be considered potentially hazardous. Immunocompromised persons, alcoholics, persons with chronic liver disease and pregnant women may require additional attention, and health care providers can play an important role in providing information about food safety. These populations should avoid undercooked meat, raw shellfish, raw dairy products, French-style cheeses and unheated deli meats [114]. [Pg.31]

Fujiki, M. 1963. Studies on the course that the causative agent of Minamata disease was formed, especially on the accumulation of the mercury compound in the fish and shellfish of Minamata Bay. Jour. Kumamoto Med. Soc. 37 494-521. [Pg.429]

The first cases of ASP were identified after an outbreak associated with eating cultivated mussels harvested from Prince Edward Island, Canada (Perl et ah, 1990 Todd, 1990b). Domoic acid also has been implicated in the deaths of marine mammals along the U.S. Pacific coast (Scholin et ah, 2000), and human diseases from eating shellfish contaminated with domoic acid have been anecdotally reported in the U.S. Pacific Northwest. [Pg.168]

In the U.S., fish and shellfish caused at least one in six food poisoning outbreaks with known etiologies, and 15% of the deaths associated with these outbreaks during 1988 to 1992. This is a marked increase over the preceding decade, when seafood consumption was associated with 10% of foodborne disease outbreaks that had identified etiologies (Ahmed, 1992 Centers for Disease Control and Prevention, 1996 Lipp and Rose, 1997). [Pg.173]

Even in areas in which shellfish poisonings are endemic, cases of these diseases are substantially under-reported. McKee et al. (2001) studied the diagnosis, treatment, and reporting of CFP in Miami-Dade County, Florida. They found that physicians had little experience of recognizing the disease, were unaware of a possible treatment (i.e., intravenously administered mannitol), and were thus unable to provide information to their patients to prevent further cases of the disease. This suggests that, despite the fact that these diseases have been known for more than 150 years, the diseases... [Pg.173]

Phycotoxins accumulate in fish and shellfish because of the natural feeding habits of the respective organisms, rather than because of food handling or processing practices. The toxins causing the diseases discussed in this chapter are heat stable (Australia New Zealand Food Authority, 2001 Committee on Evaluation of the Safety of Fishery Products, 1991). Complete inactivation of saxitoxin (associated with PSP) requires at least ten minutes of exposure to 260°C dry heat. Brevetoxins (associated with NSP) were inactivated (i.e., to levels below the limit of assay detection using Japanese medaka [Oryzias latipes]) by exposure to 500°C heat for 10 to 15 minutes (Poli, 1988). Complete inactivation required 10 minutes exposure to 2760°C dry heat (Wannamacher, 2000). [Pg.179]

Verber, J. "Shellfish Borne Disease Outbreak," Food Drug Administration, Northeast Technical Services Unit, Davisville, Rhode Island, 1984 pp. 18-20. [Pg.34]

The increased incidence of food-borne diseases from shellfish contaminated with Vibrio species have brought forward renewed interest in irradiation of shellfish and other seafood. Results are very promising for clams and oysters without killing the molluscs [65]. The radiation decimal reduction dose (Dio) determined for Vibrio cholerae 01 biotype El Tor inoculated into various molluscs was 0.14 kGy [66]. Similar radiation sensitivity of this organism was found in inoculated fish fillets and shrimp tails [67]. The radiation dose to eliminate as high as 10 CFU/g Vibrio spp. in oysters was 1.2 kGy [68]. The radiation Dio value for V. cholerae 01 biotype El Tor in marine snails was 0.11 kGy [69]. [Pg.798]

Mercury. In Japan in the 1950s and 1060s, wastes from a chemical and plastics plant containing mercury were discharged into Minamata Bay. The mercury was converted to the readily absorbed methylmercury by bacteria in the aquatic sediments. Consumption of fish and shellfish by the local population resulted in numerous cases of mercury poisoning, or Minamata disease. By 1970, at least... [Pg.41]

The red alga Digenea simplex has been used for the treatment of roundworm disease for centuries. Its active principle is kainic acid. The related domoic acid is a constituent of another red alga, Chondria armata, used for the same purpose. These compounds, known as kainoids, are potent neurotoxins and excitatory amino acids. Kainoids are important tools in neurophysiological research. Domoic acids are also produced by diatoms and were responsible for the shellfish poisonings known as amnesic shellfish poisonings that occurred in Canada in 1987. [Pg.139]

Between 1956 and 1960 severe accidents related to Me-Hg, the health consequences of which were afterwards grouped under the name of Minamata disease, occurred in Japan following long-term consumption of contaminated fish and fish products. A large amount of Hg-polluted effluents (from 200 to 600 tons) reached Minamata Bay, Japan, where they accumulated not only in the bottom sediment, but also in fish and shellfish. The consumption of such foods resulted in a mass outbreak of Me-Hg poisoning [9]. [Pg.708]

IPC is also effective for pharmacology related to brain disease. It was used to analyze picolinic acid and related compounds [90], neurotoxins associated with paralytic shellfish poisoning [91], a drug candidate for treating Alzheimer s disease [92], and nicergoline, clinically used for improving brain metabolism [93]. Quaternary ammonium anticholinergics were determined in whole blood and the matrix effect was taken into account [94]. [Pg.165]

After a number of cases were seen, investigations started. At Kumamoto University research suggested that the disease was a type of heavy metal poisoning transmitted by fish and shellfish. At the same time... [Pg.113]

A major route of human exposure to algal toxins is through the consumption of contaminated seafood products. The consumption of contaminated clams, mussels, scallops, oysters, and other shellfish causes shellfish-associated diseases (ASP, AZP, DSP, NSP,... [Pg.68]

In PSP, the toxin attacks the nervous system and causes effects that are primarily neurological and include tingling, burning, numbness, drowsiness, incoherent speech, and respiratory paralysis. Symptoms of the disease develop fairly rapidly, within 0.5-2 h after ingestion of the shellfish (generally mussels, clams, cockles, and scallops), depending on the amount of toxin consumed. In severe cases respiratory paralysis is common, and death may occur if respiratory support is not provided. There is no antidote. When such support is applied within 12 h of exposure, recovery usually is complete, with no lasting side effects. In unusual cases, because of the weak hypotensive action of the toxin, death may occur from cardiovascular collapse despite respiratory support. [Pg.2212]


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