Dar seafood ppp standard
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- Bu səhifədəki naviqasiya:
- Concentrations in seafood
- Table 4.16: Reported concentrations of histamine in seafood in Australasia
- Infectious dose/dose response
- Incidence and outbreak data
- Table 4.17: Seafood-borne outbreaks due to ciguatera poisoning in Australia and the United States, 1990–2000
- Table 4.18: Ciguatera poisoning related outbreaks of food poisoning in Australia 1990–2000
- Table 4.19: Cases of ciguatoxin illness in Queensland 1965–84
Source: Extracted from M&S Food Consultants 2001. Concentrations in seafood: Fish that have been implicated in histamine poisoning include mackerel, tuna, saury, bonito, mahi-mahi, sardines, pilchards, anchovies, herring, marlin and bluefish, however some salmon species have also been implicated (Lehane & Olley 1999). Table 4.16 indicates concentrations of histamine found in a variety of seafood products. In New Zealand, Fletcher et al. (1998) found 8/107 retail samples of smoked fish in Auckland had >50 mg/kg. Histamine concentrations of >1000 mg/kg were reported from 117/405 incidents of presumptive scombrotoxicosis in United Kingdom between 1987–96 and high concentrations have also been described in tuna steaks imported from Sri Lanka (>7000 mg/kg) and from canned tuna (245 and 3900 mg/kg) (Scoging 1998). Levels of up to 1000 mg/kg were reported in fish sauces made from Stolephorus spp., a member of the anchovy family (Brillantes & Samosorn 2001; Brillantes et al. 2002). Random import sampling reveals a small percentage of samples exceed 100 mg/kg and, of those that do, most are rarely much greater than this concentration. Information from an Australian tuna cannery that each batch of frozen tuna bodies routinely did not exceed 100 mg/kg (Lehane & Olley 1999). Current regulations: A maximum level of 200 mg/kg for histamine has been established in fish and fish products in Standard 2.2.3 – Fish and Fish Products – in the Code. Ranking of hazard: Histamine is ranked as ‘moderate’ in terms of adverse health effects (Section 3, Table 3) because of its potential to be cause short-term self-limiting symptoms following acute exposure. Table 4.16: Reported concentrations of histamine in seafood in Australasia
Source: Extracted from M&S Food Consultants 2001. CiguatoxinsCiguatoxins are known to originate from several dinoflagellate algae species (predominantly Gambierdiscus toxicus) that are common to ciguatera-endemic regions in tropical waters. The ciguatoxins are lipid-soluble toxins. These are relatively inert molecules, and remain toxic after cooking and exposure to mild acidic and basic conditions. When herbivorous fish are eaten by carnivorous fish dinoflagellate toxin is converted to the more potent ciguatoxin (Durborow 1999). These toxins accumulate through the food chain, from small fish grazing on algae on coral reefs into the organs of larger top-order predators. Toxin is concentrated in the head, liver and viscera of fish (Ting et al. 1998), but concentrations are lower in the muscle, the part more usually eaten. The occurrence of toxic fish is sporadic and not all fish of a given species or from a given locality will be toxic (Benenson 1995). If fish cease ingesting the dinoflagellate the toxin will slowly be purged from the fish. Pathology of illness: Initial signs of poisoning occur within six hours after consumption and include perioral numbness and tingling (paresthesia) which may spread to the extremities, nausea, vomiting, and diarrhoea. Neurological signs include intensified paresthesia, arthralgia, myalgia, headache, temperature sensory reversal and acute sensitivity to temperature extremes, vertigo, and muscular weakness to the point of prostration. Cardiovascular signs include arrhythmia, bradycardia or tachycardia, and reduced blood pressure (FDA 2003). Ciguatera poisoning is usually self-limiting and signs of poisoning often subside within several days from onset. However, in severe cases the neurological symptoms persist from weeks to months and, in rare cases, for several years. There is a low incidence of death resulting from respiratory and cardiovascular failure (FDA 2003). All humans are believed to be susceptible to ciguatera toxins. Populations in tropical/subtropical regions are most likely to be affected because of the relatively higher frequency of exposure to toxic fishes (FDA 2003). Repeated ciguatoxin exposures are associated with more severe illness (Glaziou & Martin 1993; Katz et al. 1993). Infectious dose/dose response: Ciguatoxin-1 is the major toxin (on the basis of both quantity and total toxicity) present in fish (Murata et al. 1990; Lewis 1994), except for certain herbivorous species which accumulate mostly gambiertoxins and less polar ciguatoxins. Lehane (1999) estimated the minimum toxic dose to be ~50 ng in an adult of 50 kg weight (that is, ~1 ng/kg body weight), on the basis of outbreak data. Mode of transmission: Ciguatera poisoning is caused by eating subtropical and tropical reef fish that have accumulated naturally occurring toxins produced by marine algae. Incidence and outbreak data: Ciguatera poisoning gives rise to considerable morbidity in 25 000 to 50 000 people worldwide each year (Hahn & Capra 2003). The epidemiological patterns of ciguatera differ markedly between Australia and the United States (Table 4.17). The annual reported rate of ciguatera poisoning in Australia between 1990–2000 is 0.3182 per 100 000 population compared to the United States which has an annual rate of 0.0131 per 100 000 population (M&S Food Consultants 2001). Table 4.17: Seafood-borne outbreaks due to ciguatera poisoning in Australia and the United States, 1990–2000
Source: Extracted from M&S Food Consultants 2001; after Smith de Waal et al. 2000. In Australia, ciguatera fish poisoning usually occurs as sporadic isolated cases (Fenner et al. 1997; Lucas et al. 1997), although at least two larger outbreaks (>30 cases) have been reported (Table 4.18; Hallegraeff 1998). Table 4.18: Ciguatera poisoning related outbreaks of food poisoning in Australia 1990–2000
Source: Extracted from M&S Food Consultants 2001. The incidence of ciguatera in Australia is skewed geographically, with Queensland bearing the major burden. A wide variety of fish species have been implicated in outbreaks in Queensland (Table 4.19). Table 4.19: Cases of ciguatoxin illness in Queensland 1965–84
Source: Extracted from M&S Food Consultants 2001; after Gillespie et al. 1986. In Queensland, several thousand cases were notified to authorities over a 10-year period (Ting et al. 1998) with an estimated 1.8–2.5 per cent of the population in that state affected (Glaziou & Legrand 1994; Lehane 1999). The average incidence in Queensland during the period 1985–90 was 1.6 cases/100 000, although in coastal Queensland the annual prevalence was estimated at 33/100 000 (Capra & Cameron 1988). Forty-one cases of ciguatera poisoning in New South Wales have been reported for the period 1996–98, although the list was not comprehensive (M&S Food Consultants 2001). Due to under-reporting of this often mild illness, these data represent the minimum prevalence in New South Wales. There have also been several large outbreaks in Sydney at restaurants. In 1987, 63 people became ill after eating Spanish Mackerel (Scomberomorus commerson) which had been caught in Hervey Bay, Queensland. Concentrations in seafood: Mackerel and barracuda from mid to north-eastern Australian waters have been reported to be frequently ciguatoxic (Price & Tom 1999). Yüklə 2,7 Mb. Dostları ilə paylaş:
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