Dar seafood ppp standard
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- Noroviruses
Viral pathogensThe viral pathogens discussed here are hepatitis A and noroviruses. Hepatitis AHepatitis A virus is classified within the enterovirus group of the Picornaviridae family. Hepatitis A virus has a single molecule of ribonucleic acid (RNA) surrounded by a small (27 nm diameter), non-enveloped, protein capsid (FDA 2003). Hepatitis A virus is distributed worldwide and is usually transmitted from person-to-person via the faecal-oral route. Hepatitis A virus is excreted in faeces of infected people and can infect susceptible individuals when they consume contaminated water or foods. Water, shellfish, and salads are the most frequent sources. Pathology of illness: The incubation period for hepatitis A virus is generally 2–6 weeks, and with a sudden onset of symptoms including fever, headache, malaise, fatigue, anorexia and nausea, usually followed by vomiting and abdominal pain. When symptoms do occur, they are usually mild and recovery is complete in 1–2 weeks. Many infections do no result in clinical illness especially in children (Grohmann 1997). Less than 0.4 per cent of reported cases in the United States are fatal, usually occurring in the elderly (Sobsey et al. 1991; FDA 2003). Recovery is complete and gives lifelong immunity to further infection. Immunocomprised individuals are more susceptible to infection (Sobsey et al. 1991; FDA 2003). The mechanisms by which illness is caused are not fully understood, but viral particles are thought to replicate in the gastrointestinal tract and then the liver where they cause cellular damage. Infectious dose/dose response: The infectious dose is unknown (Bidawid et al. 2000) but is presumably similar to other RNA enteroviruses (10–100 particles; FDA 2003). Levels in seafood: Several studies have demonstrated the presence of hepatitis A virus in bivalve molluscs grown in waters subject to human faecal pollution (Table 4.7). The prevalence of contamination is typically higher in shellfish taken from waters closed for harvest, but significant rates of contamination have been demonstrated in areas open for harvest. Table 4.7: Reported incidence of hepatitis A virus in seafood
Source: M&S Food Consultants 2001. Epidemiological data: Shellfish have been associated with food-borne viral infection throughout the world. In 1991 almost 300 000 people in Shanghai contracted hepatitis and nine died after consuming cockles contaminated with hepatitis A virus (Tang et al. 1991). Hepatitis A virus has also been linked to shellfish-associated gastroenteritis in Australia (Table 4.8). The first reported case of hepatitis A virus from shellfish in Australia was attributed to under-cooked mussels from contaminated waters in Victoria. Seven out of the ten consumers who ate the mussels developed symptoms of hepatitis A (Locarnini & Gust 1978). The largest outbreak of hepatitis A in Australia occurred during 1996–97 following consumption of oysters harvested from the Wallis Lake region, New South Wales, Australia (Communicable Disease Intelligence 1997) when 444 people were affected and one died. Table 4.8: Recent outbreaks of hepatitis shellfish-associated food poisoning in Australia
Source: C Dalton, Hunter Public Health Unit, personal communication. NorovirusesNoroviruses (previously termed Norwalk and Norwalk-like viruses) are non-enveloped RNA viruses classified in the Caliciviridae family. The group is described collectively as small round structured viruses. Pathology of illness: Noroviruses cause gastroenteritis in adults and children. The illness is relatively mild and symptoms include nausea, vomiting, diarrhoea, fever and abdominal pain with an incubation period of 1–4 days, usually followed by recovery without complications (Grohmann & Lee 2003). Onset occurs 24–48 hours after infection and the acute phase of the illness generally lasts between 1 and 2 days (ICMSF 1996). Norwalk virus causes illness by invading and damaging the gastrointestinal tract. Infection may not confer long-term immunity. Human Norovirus may cause epidemic gastroenteritis amongst all age groups and may be the most significant cause of infectious intestinal illness. Attack rates for small round structured virus seafood-associated gastroenteritis in outbreaks are relatively high, with rates of 56 per cent to 89 per cent being reported (Kirkland et al. 1996; Linco & Grohmann 1980). Infectious dose/dose response: The infectious dose is unknown but presumed to be low (FDA 2003). Levels in seafood: Norovirus has been shown to accumulate in bivalve molluscs and is commonly isolated from oysters grown waters impacted by faecal contamination (Formiga-Cruz et al. 2002; LeGuyader et al. 2000). Of particular concern, a study by Schwab et al. (1998) demonstrated that depuration of oysters may result in only a limited reduction of Norovirus concentration (7% reduction following 48 h depuration, compared with 95% reduction of bacteria). Epidemiological data: Norovirus is a major cause of food-borne disease worldwide and is commonly associated with the consumption of faecally contaminated shellfish. This was first evident in 1977, when an outbreak of gastroenteritis in the United Kingdom (> 2000 cases) was linked to oysters harvested from George’s River, Sydney (Fleet et al. 2000). The oysters had been opened and frozen on the half shell prior to being exported. During 1987–2001, at least 13 outbreaks of gastroenteritis associated with Norovirus contamination of oysters were recorded in Australia (Table 4.9; Food Science Australia & Minter Ellison Consulting 2002). A major contributing factor with these outbreaks was the consumption of raw oysters following heavy rainfall, resulting in increased faecal contamination of shellfish growing areas due to sewage pollution. Table 4.9: Recent outbreaks of Norovirus virus associated with seafood consumption in Australia
Source: Adapted from Food Science Australia & Minter Ellison Consulting, 2002. Yüklə 2,7 Mb. Dostları ilə paylaş:
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