Dar seafood ppp standard

Table 4.6: Seafood food-borne illness associated with Aeromonas species

Location	No. of people involved	Suspect food	Reference
Russia	‘mass’ poisoning	Fish (pre-frozen)	Kalina 1997
United States of America	472	Oysters	Agbonlahor et al. 1982
United States of America	7	Oysters	Abeyta et al. 1986
United States of America	29	unknown (school lunch)	Kobayashi & Ohnaka 1989
Japan	4	Seafood (sashimi)	Kobayashi & Ohnaka 1989
Scotland	>20	Cooked prawns	Todd et al. 1989
England	3	Oysters	Todd et al. 1989
England	14	Cooked prawns	Todd et al. 1989
England	2	Cooked prawns	Todd et al. 1989
Switzerland	1	Shrimp cocktail	Altwegg et al. 1991
Norway	3	Raw fermented fish	Granum et al. 1998
France	10	Dried fish sauce	Hansman et al. 2000

Source: Kirov 2003.

Suspect foods have been principally seafood and oysters, or other foods consumed with little or cooking. In only one case, which was linked to ready to eat shrimp cocktail, has the isolate from the suspect food and diarrhoeal faeces been shown to be the same ribotyping (Kirov 2003). Most recently reported Aeromonas-associated outbreaks have occurred in Sweden, Norway and France (Granum et al. 1998; Hansman et al. 2000; Krovacek et al. 1995). They are however, still insufficiently documented to definitively established Aeromonas spp. as the causative agents.

Escherichia coli

E. coli are members of the family Enterobacteriaceae. The organisms are gram-negative, facultatively anaerobic rod shaped bacteria (Desmarchelier & Fegan 2003). There are currently four main types of pathogenic E. coli that have been associated with food-borne diseases: enteropathogenic E. coli (EPEC), enterotoxigenic E. coli (ETEC), enteroinvasive E. coli (EIEC) and enterohaemorrhagic E. coli (EHEC).
EPEC have been defined as ‘diarrhoeagenic E. coli belonging to serogroups epidemiologically incriminated as pathogens but whose pathogenic mechanisms have not been proven to be related either to heat-labile enterotoxins or heat-stable enterotoxins or to Shigella-like invasiveness’ (Edelman & Levine 1983).

EPEC cause characteristic attaching and effacing lesions in the intestine, similar to those produced by EHEC, but do not produce Shiga toxins. Attachment to the intestinal wall is mediated by a plasmid-encoded outer membrane protein called the EPEC Adherence Factor in type I EPEC. However, pathogenicity is not strictly correlated to the presence of the EPEC Adherence Factor, indicating that other virulence factor are involved (ICMSF 1996).

ETEC that survive passage through the stomach adhere to mucosal cells of the proximal small intestine and produce a heat-labile and/or a heat-stable toxin. The heat-labile are similar in structure and mode of action to cholera toxin (Desmarchelier & Fegan 2003).
EIEC cause a shigellosis-like illness by invading the epithelial cells of the distal ileum and colon. The bacteria multiply within the cytoplasm of the cells, causing cells destruction and ulceration. Pathogenicity is associated with a plasmid-encoded type III secretory apparatus and other plasmid-encoded virulence factors (Desmarchelier & Fegan 2003).
EHEC are a group of E. coli organisms producing Shiga toxins and a number of other virulence factors, particularly the adhesion molecule, intimin. The Shiga toxins are closely related or identical to the toxins produced by Shigella dysenteriae. Genes of the virulence factors other than Shiga toxins are located in the locus of enterocyte effacement. These virulent factors and Shiga toxins allow the organisms to attach tightly to intestinal epithelial cells, disrupting the cytoskeletal structure and signalling pathways and causing effacing lesions (Ismaili et al. 1998). Many synonyms are used to describe EHEC, including Shiga toxin-producing E. coli, Shiga-like toxin-producing E. coli, verotoxin-producing E. coli, verocytotoxin-producing E. coli, as well as E. coli O157 and E. coli O157:H7.
Pathology of illness: EPEC primarily causes illness in infants and young children in developing countries. Symptoms include watery diarrhoea, with fever, vomiting and abdominal pain. The diarrhoea is usually self-limiting and of short duration, but can become chronic (more than 14 days). EPEC is also recognised as a food- and water-borne pathogen in adults, where it causes severe watery diarrhoea (with mucus, but no blood) along with nausea, vomiting, abdominal cramps, fever, headache and chills. Duration of illness is typically less than three days (Doyle & Padhye 1989).
ETEC is another major cause of diarrhoea in infants and children in developing countries, as well as being recognised as the main cause of ‘travellers’ diarrhoea’ (Doyle & Padhye 1989). Symptoms include watery diarrhoea, low-grade fever, abdominal cramps, malaise and nausea. In severe cases, the illness resembles cholera, with severe rice-water diarrhoea and associated dehydration. Duration of illness is from three to 21 days (Doyle & Padhye 1989).
EIEC cause a dysenteric illness similar to shigellosis. Along with profuse diarrhoea, symptoms include chills, fever, headache, muscle pain and abdominal cramps. Onset of symptoms is usually rapid (<24 hours), and may last several weeks (Doyle & Padhye 1989).
EHEC infection normally results in diarrhoea like symptoms. Haemorrhagic colitis, an acute illness caused by EHEC organisms, is characterised by severe abdominal pain and diarrhoea. This diarrhoea is initially watery but becomes grossly bloody. Symptoms such as vomiting and low-grade fever may be experienced. The illness is usually self-limiting and lasts for an average of 8 days. The duration of the excretion of EHEC is about one week or less in adults, but it can be longer in children (ICMSF 1996).
Complications resulting from EHEC infections vary. About 5 per cent of haemorrhagic colitis victims may develop Haemolytic Uraemic Syndrome (European Commission 2000). This involves the rupture of red blood cells (haemolysis), subsequent anaemia, low platelet count and kidney failure. The case-fatality rate of Haemolytic Uraemic Syndrome is 3–5 per cent (WHO 1996). Shigella toxins produced by EHEC attack the lining of the blood vessels throughout the body, predominantly affecting the kidney.
However, other organs such as the brain, pancreas, gut, liver and heart are also affected and may result in further complications such as thrombotic thrombocytopenic purpura.

Infectious dose/dose response: EPEC: It is thought that only a few EPEC cells are necessary to cause illness in children (FDA 2003). Volunteer studies in adults demonstrated that illness could be caused by ingesting 10⁶–10¹⁰ cells with sodium bicarbonate to neutralise stomach acidity (Doyle & Padhye 1989).
ETEC: Volunteer studies have shown that 10⁸–10¹⁰ cells of ETEC are necessary for illness in adults (DuPont et al. 1971), although the infective dose is probably less for infants (FDA 2003).
EIEC: Volunteer studies have shown that 10⁸ EIEC cells are necessary to cause illness in adults, with the infectious dose reduced to 10⁶ when ingested with sodium bicarbonate (DuPont et al. 1971). However, the United States FDA suggest that as few as 10 cells may be needed to cause illness in adults, based on the organisms similarity with Shigella (FDA 2003).
EHEC: Investigations of known outbreaks of food-borne illness due to E. coli O157:H7 and systematic studies aimed at quantifying the dose–response relationship suggest that as few as 1–700 EHEC organisms can cause illness. The United States FDA suggests that the infective dose is of the order of 10 cells (FDA 2003).
Incidence and outbreak data: EIEC stains have been isolated from diarrhoeal cases in both industrialised and less developed countries with low frequency (Nataro & Levine 1994). Outbreaks have occurred in hospitals, on a cruise ship, and from contaminated water (Desmarchelier & Fegan 2003). ETEC stains are a major cause of diarrhoea in infants and young children in developing countries, particularly in the tropics, and are a leading cause of travellers’ diarrhoea (Doyle & Padhye 1989; Gross & Rowe 1985; Nataro & Levine 1994). EPEC stains have caused infantile diarrhoea in hospitals and nurseries in the United Kingdom and the United States (Nataro & Levine 1994; Robins-Brown 1987). In developing countries, EPEC stains are still responsible for a high incidence of sporadic infant diarrhoea.
Among different EHEC serotypes, E. coli O157:H7 is the single most important EHEC serotype that dominates the number of reported food-borne illnesses caused by EHEC. Mead et al. (1999) reported that E. coli O157:H7 caused approximately 73 000 cases of illness each year, and non-O157:H7 EHEC caused approximately 37 000 cases of illness in the United States. During 1999 to 2002, inclusive, Australia recorded 55 cases of HUS (Communicable Diseases Australia 2003).
Levels in seafood: The occurrence of strains of EPEC, ETEC and EIEC in foods is typically the result of human faecal contamination, due either to poor hygienic practices by food handlers or raw sewage contamination of waters used in the food production and processing (Desmarchelier & Fegan 2003).

There have been only isolated outbreaks of food-borne illness attributed to seafood containing EIEC and ETEC strains of E. coli (Doyle & Padhye 1989). ETEC have been detected in Brazilian seafood harvested from contaminated waters (Teophilo et al. 2002).

EHEC are normally isolated from meat, dairy and plant products (Desmarchelier & Fegan 2003). However, a low level of contamination was detected in one survey of retail fish and shellfish samples in the United States (Samadpour et al. 1994).