Dar seafood ppp standard
Table 4.3: L. monocytogenes in Australian seafood
Yüklə 2,7 Mb.
|
- Bu səhifədəki naviqasiya:
- Table 4.4: Cases of food-borne listeriosis associated with seafood
- CFU g -1 Strain serovar
- Infectious dose/dose response
- Table 4.5: Prevalence and level of contamination of seafood products with C. botulinum spores
- Product Origin % positive
Table 4.3: L. monocytogenes in Australian seafood
Source: M&S Food Consultants 2001. Key: MPN = most probable number; cfu = colony forming units. Epidemiological data: The estimated incidence of listeriosis in European countries is four to eight cases per million of the general population per year. In France, the estimated incidence of listeriosis is sixteen cases per million (general population) per year (Bille 1990). The United States estimates that approximately 8.8 people per million (general population) become seriously ill with listeriosis each year, with a fatality rate of 20 per cent. Of all the food-borne pathogens, L. monocytogenes resulted in the highest hospitalisation rate in the United States (FDA 2003). While the incidence rate is low compared to other food-borne illnesses, such as Salmonella, the mortality rate is much higher, ranging between 5 per cent and 33 per cent, and averaging 22 per cent (Rocourt & Brosch 1992). In general, the incidence of listeriosis appears to be decreasing in most countries. The estimated incidence of invasive listeriosis in New Zealand is five cases per million (average number of cases 17 per annum) of the general population per year (Anon. 1996–2001). The fatality rate in New Zealand since 1995 is approximately 17 per cent. The number of reported cases of invasive listeriosis in Australia from 1991 to 2002, inclusive, is approximately fifty seven cases per year (Communicable Diseases Australia 2003), which equates to an estimated incidence of invasive listeriosis in Australia of three cases per million of the general population per year (Sutherland & Porritt 1997). In Australia, the exact mortality rate is not known, although the data available would suggest a rate of approximately 23 per cent. A risk assessment undertaken by the United States Food and Drug Administration (2001) looked at all documented outbreaks of listeriosis internationally, including those listed in Table 4.4, and ranked fish products third behind meat and dairy products in terms of responsibility for outbreaks for which the food linkage has been identified. Table 4.4: Cases of food-borne listeriosis associated with seafood
Source: M&S Food Consultants 2001; after FAO 1999. Clostridium botulinumC. botulinum is an anaerobic, gram positive, spore-forming rod shaped bacterium that produces a potent neurotoxin. Seven types of C. botulinum, (types A-G) are recognised, grouped according to the antigenic specificities of their toxins. C. botulinum has also been classified phenotypically into Groups I-IV. This organism is ubiquitous and is found in almost all foods, whether of plant or animal origin. Spores of C. botulinum, although usually in low numbers, are widely distributed in soil, the sediments of lakes and coastal waters and in the intestinal tracts of fish and animals. Both the spores and the toxins are tolerant of freezing. Toxin is destroyed rapidly at temperatures of 75–80°C. Group I (proteolytic) spores are the most heat-resistant of all C. botulinum spores and this led to the development of the botulinum cook or ‘12D process’ for low-acid canned foods. Strains of Group I will not grow if the water phase NaCl concentration exceeds 10 per cent (aw = 0.935) while strains of Group II will not grow if the concentration exceeds 5 per cent (aw = 0.97) in the water phase. All strains of C. botulinum grow and produce toxin to about pH 5.2 under optimal conditions. Strains of Group II will not grow below pH 5.0, while strains of Group I will not grow below pH 4.6 (ICMSF 1996). Pathology of illness: Illness caused by C. botulinum can be of three types: food-borne, infant and wound botulism (FDA 2003). Food-borne botulism is caused by ingestion of preformed toxin. The mortality rate depends on the type of C. botulinum toxin ingested. Infant botulism affects infants under the age of 12 months and results from the ingestion of spores that colonise the alimentary tract and produce toxin. Botulinum neurotoxin causes muscle paralysis, beginning in the upper body and progressing downward, paralysing the chest muscles, eventually leading to asphyxiation and death. Even with treatment, 20–40 per cent of victims die (M&S Food Consultants 2001). Onset of symptoms in food-borne botulism is usually 18–36 hours after ingestion of the food containing the toxin, although cases have varied from 4 hours to 8 days. Early signs of intoxication consist of marked lassitude, weakness and vertigo, usually followed by double vision and progressive difficulty in speaking and swallowing, difficulty in breathing, weakness of other muscles, abdominal distension, and constipation may also be common symptoms (FDA 2003). All people are believed to be susceptible to the food-borne intoxication. For seafoods, botulism is most commonly associated with C. botulinum type E (Group II). C. botulinum type E is capable of growth and toxin production at refrigeration temperatures (≥ 3.3°C) but generally needs weeks of growth to produce sufficient amounts of toxin to cause food-borne illness (Lyon & Reddmann 2000). This is significantly greater than the shelf life generally observed for seafood. Botulism is a concern, however, when processes are used to extend the shelf life, such as canning and vacuum packing. If the C. botulinum spores survived treatment processes prior to packaging, they have the ability to proliferate and produce toxin, especially if the food is subjected to temperature abuse. Infectious dose/dose response: A very small amount (a few nanograms) of botulinum toxin can cause illness (FDA 2003). As little as 0.1–1.0 µg of type A toxin has been found to cause death in humans (ICMSF 1996). Levels in seafood: The aquatic environment is frequently contaminated with C. botulinum spores and therefore fish are often contaminated. A large number of surveys have been conducted, including those for seafoods at retail (Table 4.5). The incidence and level of contamination of prepared fish in Europe and Asia appears to be much lower than that in North America, but fish from Scandinavia and the Caspian Sea appear to be exceptions (Dodds 1993). Only a limited amount of data are available on the prevalence of C. botulinum in Australia. C. botulinum types A, B and C have been isolated from soils and waterways and have caused illness in domestic animals (Szabo & Gibson 1997). C. botulinum type B was found in two marine muds from Tasmania (Szabo & Gibson 1997). In a study specifically designed to isolate C. botulinum type E, Christian (1971) found no evidence from 528 samples of soils, marine muds, fish intestines and potato washings from Tasmania, New South Wales and Queensland. Gibson et al. (1994) examined 368 samples from various Australian coastal marine, harbour and estuarine sediments and found no samples positive for the presence of the organism. Table 4.5: Prevalence and level of contamination of seafood products with C. botulinum spores
Source: M&S Food Consultants 2001; after Dodds 1993. Key: MPN = most probable number. Epidemiological data: Botulism caused by consumption of commercial foods is rare, with most cases involving non-commercial foods (M&S Food Consultants 2001). Outbreaks are generally associated with improperly canned food (usually home canned) and semi-preserved seafoods including smoked, salted (particularly when uneviscerated) and fermented fish. Outbreaks of botulism have been reported due to consumption of contaminated mussels in Portugal (Lecour et al. 1988); uneviscerated salted mullet fish (Faseikh) in Egypt, in April 1991 (Weber et al. 1993); hot-smoked Canadian whitefish in 1997 (Korkeala et al. 1998). Ten outbreaks of botulism associated with seafoods have occurred in the United States over the period 1988–98 (Bean et al. 1996; Olsen et al. 2000). Three deaths were reported in New York city from consumption of contaminated seafoods (Wallace et al. 1999); another two deaths reported from botulinum type E toxin associated with eating ‘kapchunka’, a salted ungutted whitefish dish (Badhey et al. 1986) and a further 8 cases occurred in New York and Israel involving the same food (Telzak et al. 1990). In Canada 61 outbreaks occurred in the period 1971–84, most (113/122) cases involving native peoples eating raw, parboiled or ‘fermented’ meats from marine mammals. A similar pattern of illness occurs in Alaska. Fermented salmon eggs or fish were responsible for 23 per cent of these outbreaks (Hauschild & Gauvreau 1985). In 1978 (United Kingdom) and 1982 (Belgium) there were two outbreaks of botulism from canned salmon. In the United Kingdom, two people died and two recovered (Murrell 1979) while in Belgium, one died and one recovered (Anon. 1982). There were also a number of outbreaks from smoked, vacuum-packed whitefish in United States in 1963; in all there were 25 cases of botulism and 10 deaths (Anon. 1963). In New Zealand, there have been two cases of illness (one death) due to botulism type A involving home-bottled fermented mussels and watercress, a traditional Maori food Hauschild (1993). There have been no reported cases of food-borne botulism in Australia since national notification commenced in 1991 (Blumer et al. 2003). From 1942–83 there were five reported outbreaks of botulism in Australia (Hauschild 1993), of which one (two cases) was linked to consumption of Australian canned tuna (Murrell 1979). Yüklə 2,7 Mb. Dostları ilə paylaş:
|