Dar seafood ppp standard
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- Appendix 4
- Bacterial pathogens
- Vibrio cholerae
- Vibrio parahaemolyticu s
- Vibrio vulnificus
Fish and fish productsTable 3.9: Consumption of finfish (fillets/gutted/whole for cooking) in Australia, by gender and age
Table 3.10: Consumption of canned finfish in Australia, by gender and age
Table 3.11: Consumption of smoked finfish in Australia, by gender and age
Table 3.12: Consumption of fish roe in Australia, by gender and age
Appendix 4Hazard identification/hazard characterisationThis Appendix provides a brief description of the hazards associated with seafood along with information on the nature, severity and duration of adverse health effects resulting from exposure to these hazards. The incidence of illness and hazard levels detected in various seafood are also described. The information presented in this attachment has largely been extracted from the ‘Seafood Food Safety Risk Assessment’ conducted by M&S Food Consultants, who were commissioned by Seafood Services Australia in 2001 to undertake a national seafood risk assessment. Other data was derived from FSANZ’s ‘Shellfish Toxins in Food: Toxicological Review and Risk Assessment’, 1999, which was prepared as part of Proposal P158 – review of the maximum permitted concentrations of non-metals in food. Bacterial pathogensThe bacterial pathogens discussed here are Vibrio spp., Staphylococcus aureus, Salmonella species, Listeria monocytogenes, Clostridium botulinum, Aeromonas hydrophila and Escherichia coli. Vibrio spp.Vibrio species are ubiquitous in the aquatic environment, with a small number of species/strains able to cause human disease (Morris 2003). Vibrios are described as gram-negative, facultatively anaerobic, halophytic (salt-loving), motile curved rods with a single polar flagellum (ICMSF 1996). Vibrio choleraeDescription: The temperature range for V. cholerae growth is 10–43°C, the minimum aw for growth is as low as 0.97 and the pH range for growth is 5.0–9.6. V. cholerae can survive in foods for periods up to a month or more as long as the aw is sufficiently high (ICMSF 1996). V. cholerae is sensitive to acid and dry conditions and so survival under these conditions is generally <12 hours at room temperature. There are three main serological groupings of V. cholerae; namely O1, O139 and non-O1/non-O139. Toxigenic V. cholerae O1 and O139 are the causative agents of cholera, a food-borne illness with epidemic and pandemic potential. Non-O1/non-O139 V. cholerae do not carry the virulence factors necessary to cause epidemic cholera but have been implicated as causes of diarrhoeal disease, wound infections and, in susceptible populations, septicaemia (Morris 2003). V. cholerae O1 is divided into two serotypes, Indaba and Ogawa, and two biotypes, classic and El Tor (Prescott et al. 1999). The classic biotype, such as the V. cholerae strain first isolated by Robert Koch in 1883, was more prevalent in cholera outbreaks before 1960, whereas the El Tor biotype has been more frequently seen since that time (Madigan et al. 1997). Pathology of illness: Illness in humans is initiated by adherence of toxigenic O1 and O139 V. cholerae cells to the surface of the small intestine, where they are not invasive but produce cholera enterotoxin, choleragen. The action of the toxin on mucosal cells leads to hypersecretion of salts and water. Loss of water can be as much as 1 L/h and can lead to collapse and death. Initial symptoms include mild diarrhoea, abdominal pain and anorexia and are rapidly followed by severe diarrhoea (classic rice water stools), with rapid loss of body fluids and salts. Without treatment cholera can be fatal, but in otherwise healthy and well-nourished patients, recovery occurs in 1–6 days. V. cholerae non-O1 and non-0139, cause milder symptoms (ICMSF 1996). The incubation period ranges from several hours to 5 days and depends in part on the dose. Onset of illness can be sudden or there may be premonitory symptoms such as anorexia, abdominal discomfort and diarrhoea. Stomach acidity has a protective effect. Individuals who are achlorhydric (low stomach acidity) because of medication (such as antacids) or other reasons, are more susceptible to infection. Individuals of blood group O are also more susceptible to infection, although the mechanism of this susceptibility is not known (Oliver & Kaper 1997). Individuals with cirrhosis of the liver are susceptible to non-O1 V. cholerae bacteraemia (Lin et al. 1996). Infectious dose/dose response: When ingested with food (or after neutralisation of stomach acidity) the infectious dose of V. cholerae O1 and O139 in healthy adult volunteers is estimated to be 103 – 104 cells (Levine et al. 1981; Kothary & Babu 2001). Lower inocula correlated with a longer incubation period and diminished severity of symptoms. Attack rates at these doses were >60 per cent. Analysis of outbreaks suggests V. cholerae O1 and O139 may be infectious at doses as low as 102 to 103 CFU (M&S Food Consultants 2001). V. cholerae non-O1/non-O139 strains appear to have a much higher infectious dose of between 106 and 109 bacteria (Cash et al. 1974; Oliver & Kaper 1997; Kothary & Babu 2001). Levels in seafood: Only V. cholerae non-O1/non-O139 and non-toxigenic V. cholerae O1 strains have been isolated from brackish and estuarine waters and oysters in Australia (Desmarchelier 1997; Eyles & Davey 1984; 1988). Epidemiological data: Seven pandemics have been recorded worldwide since 1817 (Morris 2003). Cholera remains epidemic in many parts of Central and South America, Asia, and Africa (CDC 1995). In 2001, 58 countries officially reported a total of 184 311 cases and 2728 deaths to the World Health Organisation (WHO 2002). Cholera is generally transmitted via ingestion of faecally contaminated foods and waters (Centre for Disease Control 1995). Outbreaks of cholera have been associated with consumption of seafood including oysters, crabs and shrimp (Oliver & Kaper 1997). For example, a seafood-associated outbreak of cholera in Hong Kong was linked to contaminated seawater in fish tanks used for holding live crustacea (Kam et al. 1995). The incidence of cholera in Australia is low, with an average of less than 4 reported cases per annum in the period 1991–2002 (inclusive) (Communicable Diseases Australia 2003). The majority of reported cases in Australian are generally acquired overseas (Kraa 1995). An outbreak occurred in Australia in 1999 due to consumption of crayfish contaminated with V. cholera non-O1/non-O139, resulting in 10 cases of illness (Appendix 2). Vibrio parahaemolyticusDescription: V. parahaemolyticus is distributed worldwide in inshore marine waters and is mesophilic. The temperature range for growth is 5–43°C, the minimum aw for growth is as low as 0.94 and the optimal NaCl concentration for growth is 3 per cent (aw = 0.980). V. parahaemolyticus will grow in the pH range of 4.8–11 (ICMSF 1996). Pathology of illness: Illness is caused when the ingested organism attaches itself to an individual’s small intestine and secretes a toxin. V. parahaemolyticus causes gastroenteritis and symptoms include watery diarrhoea, abdominal cramps, nausea, vomiting, headache, fever and chills. Onset of illness is generally after 4–96 hours with a mean of 15 hours. Illness usually resolves in three days and mortality is normally very low. A more severe dysenteric form of illness that may need hospitalisation has been reported in India, United States (2 cases) and Bangladesh (Twedt 1989). Severe illness is rare and usually occurs in people with weakened immune systems or chronic liver disease. In these cases, infection can lead to septicaemia (Morris 2003). Not all strains of the organisms are pathogenic. There appears to be a lack of correlation between pathogenicity and serotype of V. parahaemolyticus isolates. Virulence correlates with the ability to produce a thermostable direct haemolysin termed the Kanagawa Phenomenon haemolysin. Kanagawa Phenomenon negative strains appear to be non-pathogenic (Twedt 1989; Oliver & Kaper 1997). Kanagawa Phenomenon haemolysin is heat-stable and therefore remains active even after cooking (Twedt 1989). Infectious dose/dose response: Human volunteer studies have established an infectious dose for KP-positive strains between 2 105 and 3 107 cfu (Takikawa 1958; Sanyal & Sen 1974). Diarrhoeal illness was not caused by ingestion of up to 2 1010 cfu of a KP-negative strain (Centre for Food Safety and Applied Nutrition 2001). However, the level of V. parahaemolyticus in oysters from beds implicated in the United States 1997 and 1998 outbreaks was less than 200/g, indicating that human illness can occur at lower levels than currently suspected (Morbidity and Mortality Weekly Reports 1999). Levels in seafood: Studies have demonstrated a seasonal and geographical variation in the concentration of V. parahaemolyticus in marine waters, with higher numbers detected in samples collected during the warmer months (DePaola et al. 1990; Cook et al. 2002; Gooch et al. 2002). This is in contrast to many other bacterial pathogens (such as Salmonella, pathogenic E. coli and Campylobacter) where survival is inversely related to temperature (Obiri-Danso & Jones 1999). Therefore, concentrations of Vibrio spp. do not always correlate with traditional faecal indicator organism concentration. Concentrations of V. parahaemolyticus have been observed to be >100 times higher in oysters compared with the surrounding coastal water (DePaolo et al. 1990). In a study in the United States, the concentration of V. parahaemolyticus in freshly harvested oysters was typically between 200 and 2000 CFU/g, with a prevalence of up to 21% (Kaufman et al. 2003; Nordstrom et al. 2004). The prevalence of V. parahaemolyticus is usually lower in crustacea and finfish than in oysters (Table 4.1). Table 4.1: Incidence of V. parahaemolyticus in seafood
Source: M&S Food Consultants 2001. Key: MPN = most probable number; cfu = colony forming units. A study by Gooch et al. (2002) investigated the ability of V. parahaemolyticus to grow in oysters, post-harvest. After 24 hours storage at 26C there was a 790-fold increase (2.9 log CFU/g) in concentration, demonstrating V. parahaemolyticus can multiply rapidly in unrefrigerated oysters. After 14 days of refrigeration, there was a six-fold decrease (0.8 log CFU/g) of V. parahaemolyticus. Others have reported long-term survival of V. parahaemolyticus on chilled and frozen fish fillets (Vasudevan et al. 2002). Epidemiological data: There have been a number of large outbreaks of V parahaemolyticus gastroenteritis in Australia (Appendix 2). In 1990 an outbreak affecting more than 100 people, one of whom died, was linked to fresh, cooked prawns from Indonesia. In 1992 there were two outbreaks affecting more than 50 people linked to the same wholesale supplier of cooked prawns (Kraa 1995). One death due to V. parahaemolyticus gastroenteritis associated with consumption of oysters was reported in 1992 (Kraa 1995). In the United States and Europe, most gastroenteritis-related outbreaks have been due to the consumption of raw molluscs (oysters and clams) or cooked crustaceans (shrimp, crab and lobsters). In Japan, South-East Asia, Africa and India, raw fish has been implicated. Vibrio vulnificusDescription: The temperature range for V. vulnificus growth is 8–43°C, the minimum aw for growth is as low as 0.96 and the optimal NaCl concentration for growth is 2.5 per cent (aw = 0.983). The pH range for growth is 5–10 (ICMSF 1996). Pathology of illness: Disease caused by V. vulnificus is characterised by a 24-hour incubation period, followed by signs of sepsis, including fever, chills and nausea (Potasman et al. 2002). Symptoms typical of gastroenteritis, abdominal pain, vomiting and diarrhoeal are less common. V. vulnificus is highly invasive and produces a number of virulence factors which may cause tissue damage (including lesions). Again, immunocompromised individuals and those suffering from chronic liver disease are particularly susceptible to V. vulnificus infection. V. vulnificus can also lead to infection by directly contaminating open wounds during swimming, shellfish cleaning and other marine activities (Centre for Disease Control 1993). Infectious dose/dose response: The infectious dose is not known. It has been suggested that the infectious dose may be very low in susceptible individuals (Oliver & Kaper 1997) and analysis of oysters associated with V. vulnificus primary septicaemia indicates that ca. 103/g of oyster or higher were associated with infection (Jackson et al. 1997; Tamplin & Jackson 1997). Levels in seafood: Levels reported in seafood range from 15 – 6 104/g (Table 4.2; Oliver 1989; Oliver & Kaper 1997). Although human illness has only been associated with consumption of oysters, V. vulnificus has been isolated in high numbers (>106 cfu/g) from intestinal contents of fish, shrimp and prawns, with low numbers being detected in muscle (DePaola et al. 1994; Hoi et al. 1998; Thampuran & Surendran 1998; Berry et al. 1994; Prasad & Rao 1994). Numbers of V. vulnificus in seawater and seafood vary according to season (Ruple & Cook 1992; DePaola et al. 1994; Motes et al. 1998). In Chesapeake Bay, United States, V. vulnificus was not detected in any samples collected during February and March (water temperature <8˚C) but was found in 80 per cent of the water samples collected during May, July, September, and December (water temperature >8˚C), with concentrations ranging from 3.0 101 – 2.1 102/mL. Isolation from oysters was demonstrable when water temperatures were 7.6˚C, with concentrations ranging from 1.0 103 – 4.7 104/g (Wright et al. 1996). High V. vulnificus levels in oysters (>103/g) are also associated with intermediate salinities (5 to 25 ppt), with numbers generally being lower in oysters from water salinities above 28 ppt (Motes et al. 1998). V. vulnificus has been isolated from Australian waters (Myatt and Davis 1989) and cases of wound sepsis have been reported (Maxwell et al. 1991). A 1990 survey in New South Wales found 40 per cent of oysters were contaminated with V. vulnificus (McAnulty 1990). However, there is little published data on the levels of V. vulnificus in Australian seafoods or seawater. As indicated in Table 4.2, V. vulnificus has been found at ‘low levels’ in oysters in Australia (Bird and Kraa 1995). Table 4.2: Incidence of V. vulnificus in seafood
Source: M&S Food Consultants 2001. Key: MPN = most probable number. Epidemiological data: In the United States between 1988 and 1996, 422 V. vulnificus infections from 23 states were reported. Of these reported cases, 45 per cent were wound infections, 43 per cent were primary septicaemia infections, 5 per cent were gastroenteritis infections and 7 per cent of infections were undetermined. Of those with primary septicaemia, 96 per cent had consumed raw oysters. The fatality rate of individuals with primary septicaemia was 61 per cent with underlying liver disease associated with fatal outcome (Shapiro et al. 1998). An outbreak of V. vulnificus infection associated with consumption of raw oysters was documented in 1992. All cases were aged 50–74, suffered from chronic liver disease and presented with primary septicaemia; there were 2 deaths (Kraa 1995). Between 1987–2001, five individual incidents of V. vulnificus infection associated with consumption of raw oysters were reported, leading to four deaths, of which were primarily individuals with chronic liver disease (Food Science Australia & Minter Ellison Consulting 2002). Yüklə 2,7 Mb. Dostları ilə paylaş:
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