Source: https://veteriankey.com/food-chain-and-health-hazards/
Timestamp: 2019-04-26 09:40:35+00:00

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• if something goes wrong at a given point in the food chain, it can negate any successes achieved at other points, so all the activities along the whole food chain must be integrated and coordinated.
The strong inter-relationship between food production chain and food quality/safety is being increasingly recognized and accepted by major food retailers (e.g. supermarket chains). By doing so, they represent a commercial motor for the vertical integration of food producers. Examples of good integration include the poultry chain and the milk/dairy chain, in which a single company often owns all production phases: animal feed–animal farms–primary food production–food processing–retailing.
In such systems, approaches to associated public health hazards and their controls can be, and often are, similarly integrated. The main phases of the food production and associated hazards are illustrated in Fig. 1.1 using the example of the meat chain. When considering the complexity of the chain, diversity of the hazards and necessity of understanding their inter-relationship, it becomes clear that the approach to protection of the consumer’s health must be science-based and multidisciplinary. In the following chapters, essential information required for assessing the public health risks and their controls along the food chain will be given, leading to the final chapter summarizing the framework for longitudinal and integrated food safety assurance.
Fig. 1.1. The nature of the food chain and associated hazards.
1. Invasive infection, in which the organism invades and penetrates intestinal mucosa.
2. Toxico-infection, in which the organism produces toxin while in the intestinal tract.
3. Intoxication, in which the organism produces specific toxins or toxic metabolite(s) in the food that is ingested.
Classification of disease by symptoms may be misleading from an aetiological point of view, because more than one organism can be responsible for similar clinical symptoms. For example, haemolytic uraemic syndrome (HUS) can be caused by E. coli O157, other stx-producing E. coli, Shigella and Campylobacter.
Agents for food-borne disease have generally been recognized because of the occurrence of large numbers of cases from a common source and with similar symptoms (a disease outbreak) or clusters of cases (two to a few individuals). During outbreaks, epidemiological investigators examine suspect foods, recover bacterial isolates and compare those with patient isolates using genetic typing techniques (commonly Pulsed Field Gel Electrophoresis). However, most food-borne illness occurs sporadically – where only one patient has symptoms. Investigation of disease is more difficult for sporadic cases, as isolating the causative organism from food is problematic. Sporadic cases constitute most of the worldwide food-borne disease burden.
The source of bacterial pathogens existing in food includes many harvest or post-harvest sources and may not be confined to the food itself (livestock, livestock products or plants). Although some food-borne bacterial pathogens are zoonotic agents (e.g. Salmonella, Listeria), their presence on/in food is not necessarily a direct result of their spread from livestock during harvest. Food handlers can be a source of food-borne pathogens, as they may harbour some pathogens asymptomatically, be infected or have hands contaminated from other sources (e.g. Listeria from drains). To establish a zoonotic link, matching isolates should be recovered from the animal in question, which is not often possible. Contamination of food by food handlers via faeces, vomit, skin lesions or mucus is a likely source of many food-borne bacteria, while viral pathogens may originate from human faeces or vomit. Fomites may also be vehicles for the spread of bacterial pathogens to foods.
An important group of Gram-negative bacteria found in the GIT of humans and animals are classified in the bacterial family Enterobacteriaceae. Genera from this family, which can be food-borne pathogens, are Salmonella, Escherichia, Shigella and Yersinia.
Measures to control specific food-borne pathogens, discussed below, do not generally include on-farm hygiene measures, nor adjustment to food processing parameters.
Campylobacter jejuni (the most common species) and C. coli cause the invasive infection campylobacteriosis. The pathogen is found in the GIT of livestock, poultry and other animals including pets (Blaser et al., 1979; Stern and Line, 2000), so is commonly spread by faeces and faecally contaminated water. Asymptomatic faecal carriage occurs occasionally in humans. Campylobacter cause between 5 and 14% of all diarrhoeal illness worldwide (Anon., 2000a, b), and are the most common laboratory isolates from humans with gastroenteric symptoms in most developed countries (Table 1.1).
Campylobacter are spiral, curved or winged motile rods (Smibert, 1984). Campylobacter have atopt of between 37 and 45°C, but do not grow well, if at all, below 25°C. Campylobacter is micro-aerophilic, with optimal growth in 10% CO2 and requiring a low O2 concentrations of around 5%. They are salt-sensitive, being mostly inhibited by 2% NaCl. The pathogen grows best at pH 6.5 to 7.5. Campylobacter survive in foods at 4°C, but are sensitive to drying and heating (ICMSF, 1996).
The incubation period is typically 2 to 5 days (Stern and Line, 2000). Symptoms include fever, malaise, abdominal pain (can be severe, mimicking appendicitis), diarrhoea – which can be bloody (Blaser et al., 1979) and headache. Sequelae include reactive arthritis, while Guillain Barré syndrome may develop 1 to 3 weeks after C. jejuni infection (Stern and Line, 2000). HUS also can occur. Campylobacteriosis is more common in children or young adults than in others. The disease is self-limiting and typically lasts up to 10 days, but individuals can shed the pathogen for up to 2 months post-resolution of symptoms (Anon., 1992a). Infants and young adults are most at risk.
Table 1.1. Incidence of laboratory isolations of selected pathogens from humans with disease symptoms, by country (isolations per 100,000 population).
Campylobacter jejuni invades the large and small intestine (Beery et al., 1988), produces toxin and forms abscesses in the crypts of the villi. Infection of the appendix may occur.
As the infectious dose appears low, around 500 CFU (colony-forming units), growth of the pathogen in food is not necessary. Foods that have caused campylobacteriosis include unpasteurized milk, water and undercooked poultry. Foods which appear to have been cross-contaminated from known Campylobacter sources are often implicated.
1. Cook poultry and meats thoroughly.
2. Pasteurize milk and dairy products; don’t consume unpasteurized products.
3. Prevent cross-contamination of heat-treated foods.
4. Prevent cross-contamination of utensils.
5. Use only potable water in food production; consume only potable water.
6. Control birds and rodents.
Salmonella causes two types of food-borne human disease. First, salmonellosis is most commonly caused by S. enterica subsp. typhimurium or S. enterica subsp. enteritidis (World Health Organization, 1995; D’Aoust, 2000). Secondly, S. enterica subsp. typhi and S. enterica subsp. paratyphi are the causes of typhoid fever or paratyphoid fever, respectively (Anon., 1992c). Salmonella can replicate both inside the vacuoles of host cells (Garcia-del Portillo and Finlay, 1994) and in the external environment. Salmonella are the second most common pathogens isolated from humans with gastroenteric disease in developed countries (Table 1.1).
Salmonella are non-sporing, motile rods, and are facultatively anaerobic (Le Minor, 1984). Salmonella have a topt of 37°C, but this is strain-dependent; growth occurs between 5 and 47°C. Grow best at pH 7, but can grow in relatively acidic conditions, pH 4.0 to 5.4. Nitrite and high salt concentrations are inhibitory at low pH. Salmonella survive very well in dried foods, particularly those with protective fats and proteins. Salmonella are not heat-tolerant, so will be destroyed by thorough cooking.
Salmonella typhimurium and S. enteritidis occur in the GIT of animals, including livestock. The pathogen is spread by faeces to the environment and to foods. Faecal–oral transmission is normal, but person-to-person transmission can occur, particularly in institutions.
The incubation period is typically 6 to 48 h (Yoshikawa, 1980). Symptoms include mild fever, nausea, vomiting, headache, aching limbs, abdominal pain and diarrhoea lasting from a few days to one week. The disease is self-limiting, but can be severe in young, elderly or otherwise IC (immunocompromised) people (Anon., 1992c; World Health Organization, 1995).
Salmonella invade epithelial cells in the ileum and proliferate in the lamina propria. Profuse, watery diarrhoea results. Some isolates produce a heat-labile enterotoxin, which initiates diarrhoea. Sequelae include postenteritis reactive arthritis and Reiter’s syndrome (D’Aoust, 2000), and systemic infection can result. Individuals can develop carrier status of up to 6 months in duration (Anon., 1992c).
The infectious dose varies, from only a few CFU to >105 CFU, so growth of the pathogen in foods has not been a factor in all cases of food-borne salmonellosis, but appears to have been in some. Foods known to have been vehicles of salmonellosis include poultry, eggs, meat, milk, chocolate, coconut and frog legs. However, any faecally contaminated food can be implicated. As Salmonella are heat sensitive, raw or undercooked foods are more likely to cause infection.
2. Pasteurize milk and dairy products; avoid consumption of unpasteurized products.
4. Avoid undercooked or raw eggs.
5. Store heat-treated foods at <4°C or >60°C to prevent growth.
6. Reduce carriage of livestock by vaccinating or dosing with antibiotics or probiotics.
7. Exclude infected or carrier-status individuals from handling food.
8. Control rodents and insects.
9. Dispose of sewage in a sanitary manner.
Salmonella typhi and S. enterica subsp. paratyphi cause the systemic diseases typhoid fever and paratyphoid fever, respectively. These pathogens occur in human faeces, and are spread via human faeces to the environment and to foods. Person-to-person transmission is common.
The disease symptoms of typhoid and paratyphoid fevers are dissimilar to those of enteric salmonellosis. The incubation period is typically 10 to 20 days, but ranges from 3 to 56 days. Symptoms include fever, headache, abdominal tenderness, constipation, rose-coloured spots on the body, possibly followed by diarrhoea.
Salmonella penetrate the intestinal epithelium, possibly proliferating in macrophages and polymorphs, pass into mesenteric lymph nodes, liver or spleen then cause septicaemia. Peritonitis and subsequent death can occur. Ulceration of the ileum can occur if organisms multiply in the bile of the gall bladder and cause reinfection.
The infectious dose ranges from 103 to 106 CFU. Any food could be a vehicle of infection if contaminated with human faeces. Foods known to have been vehicles of typhoid fever include raw milk, shellfish and meat. However, typhoid fever is predominantly spread by water contaminated with human faeces.
1. Use only potable water in food production; consume only potable water.
2. Dispose of sewage in a sanitary manner.
3. Avoid consumption of raw shellfish.
4. Use good personal hygiene practices when handling foods.
6. Prevent cross-contamination of heat-treated foods.
8. Give antibiotic therapy to prevent long-term carrier status developing.
Escherichia coli O157 causes toxico-infections, producing enteric and/or systemic illnesses. Although this disease is relatively infrequent (Table 1.1) it can have severe consequences, including haemorrhagic colitis (HC), haemolytic uraemic syndrome (HUS) and thrombotic thrombocytopaenic purpura (TTP).
Shiga toxin (stx)-producing E. coli O157 are carried in the GIT of healthy livestock. Cattle are a suspected main reservoir (Chapman et al., 1992), but the organism can be found in the GIT of sheep, deer, goats, poultry, horses, dogs, rats, flies, birds and humans. Asymptomatic faecal carriage occurs in both animals and people. Other stx-producing E. coli are also carried extensively in the GIT of healthy cattle, but are less common human pathogens and, to date, have only rarely been proved to be food-borne. The most common route of E. coli O157 infection is person-to-person, but other routes of infection include food-borne and animal-to-person.
E. coli O157 are non-sporing, facultatively anaerobic rods that are usually motile (Ørskov, 1984). The organism is a member of the family Enterobacteriaceae, so grows optimally at 37°C and pH 7.0 (Anon., 1992b). Although the organism does not grow at refrigeration temperature, it survives well in refrigerated food. Growth can occur as low as 7 to 8°C, in the pH range 4.4 to 9.0, and in 6.5% NaCl. E. coli O157 are similarly acid resistant as serovars of E. coli, most of which appear to be quite acid tolerant. E. coli O157 are not heat-tolerant, so will be destroyed by thorough cooking. E. coli O157 survive well in livestock wastes and soils (months, up to 1 year).
The incubation period is typically 3 to 8 days, and ranges from 1 to 11 days (Anon., 1992b). The infectious dose appears extremely low, around 10 to 100 CFU. Symptoms are very varied, including watery diarrhoea and HC with severe abdominal pain, sometimes accompanied by vomiting. HUS can occur, with symptoms of kidney failure, reduced white cell count and anaemia (Nataro and Kaper, 1998). TTP typically has similar symptoms to HUS, but the CNS is also involved, and bleeding into tissues and organs can develop, with blood clots in the brain. Young children are at greatest risk of HUS. HUS typically lasts days or weeks, and requires hospitalization, blood transfusions and dialysis. Coma and death occur frequently in target populations of the young (HUS) and the elderly (TPP) (Nataro and Kaper, 1998).
Ingested bacteria adhere to the large intestine where they probably proliferate and produce stx 1 and/or stx 2. Stx may be translocated to target organs (kidneys, CNS) by unknown means, and to cells containing active binding sites for stx. Stx binds to the cell surface, moves through the cell membrane to the endoplasmic reticulum and halts protein synthesis, causing cell death.
As the infectious dose can be extremely low, growth of the pathogen in foods is not necessary. Foods that have been proven vehicles of infection include meats, particularly if minced or comminuted and then undercooked, e.g. beefburger (Anon., 1992b). Ready-to-eat meats including salami, jerky and cooked meats have caused outbreaks, as have unpasteurized apple juice, unpasteurized milk, unpasteurized cheese, yoghurt, salad sprouts, well water and lake water (Park et al., 1999).
1. Use GHP and HACCP in meat production.
2. Cook meat thoroughly until >72°C in the centre, instantaneously.
3. Pasteurize juice and dairy products; don’t consume unpasteurized products.
4. Prevent cross-contamination of heat-treated foods.
5. Exclude infected individuals from handling foods.
6. Use only potable water in food production; consume only potable water.
7. Prevent young children contacting livestock and farm environments.
8. Avoid eating in areas that could be contaminated with animal faeces. Wash hands thoroughly before eating.
9. Do not use organic waste or faecally-contaminated water on ready-to-eat crops.
10. Control rodents, insects and birds.
Shigella sonnei, S. dysenteriae, S. boydii and S. flexneri cause the invasive infection shigellosis. Shigella are found only in the GIT of humans and higher primates, where they are mostly carried asymptomatically (Lampel et al., 2000). Transmission occurs via the faecal–oral route and person-to-person.
Shigella are non-sporing, motile rods, and are facultatively anaerobic. The organism is a member of the family Enterobacteriaceae (Rowe and Gross, 1984), so grows in the range of 6 to 48°C, but topt is 37°C and pH 7. Shigella can grow in 5% NaCl.
The incubation period is typically 48 h, but ranges from 1 to 7 days (Anon., 1992d). Shigella causes a variety of symptoms, from mild to severe. Symptoms include mild diarrhoea, typically lasting for one to two weeks, and are self-limiting (Anon., 1992d). Dysentery is more severe, with high fever, chills and dehydration. Convulsions can occur in children under 4 years old. Sequelae include HC, neurological symptoms and HUS. Severe cases of dysentery can require hospitalization, and blood transfusion or kidney dialysis may be necessary in the case of HUS. Individuals can develop carrier status, lasting for months.
Shigella proliferate within epithelial cells in the ileum and colon, producing the milder symptoms. If surfaces of the epitheliae become inflamed, causing necrosis and ulceration, red blood cells and serum proteins can subsequently infiltrate the lumen, producing dysentery.
As the infectious does is typically ~100 CFU, but may be as few as 10 CFU in susceptible individuals, growth of the pathogen in food is not necessary. Shigellosis is not necessarily a zoonosis; any food requiring substantial handling can be a non-specific vector. Foods involved are raw foods including fruits and salads, as well as food handled before incorrect cooking or after cooking (chicken, shellfish, egg products, puddings). Poor hygiene amongst infected/carrier food handlers and faecal contamination of water supplies are common factors contributing to outbreaks.
1. Use good personal hygiene practices when handling foods.
2. Exclude infected or carrier-status individuals from handling food.
3. Use only potable water in food production; consume only potable water.
4. Dispose of sewage in a sanitary manner.
5. Cook food thoroughly to inactivate Shigella on raw food.
Vibrio cholerae O1 classic biotypes, El Tor biotype and V. cholerae O139 are the cause of cholera, a toxico-infection (Anon., 1992e). V. cholerae primarily inhabit marine water, estuaries and salt marshes. The most common source of cholera is faecally contaminated water (Kaysner, 2000).
All Vibrio are facultatively anaerobic halophilics, straight or curved, motile rods. Seawater or 2 to 3% (range 0.5 to 10%) NaCl is required for survival and growth of most Vibrio (Kaysner, 2000). Growth occurs from 5 to 43°C, but growth tmin in waters is around 10 to 19°C. Growth occurs over a wide pH range, from pH 4.8 to 11.0, but they are alkalophilic, with pHopt of 7.8 to 8.6. Vibrio are sensitive to heat: cooking to 65°C kills this pathogen.
The incubation period is typically 6 h to 5 days (Kaysner, 2000). Symptoms include profuse watery diarrhoea with ‘rice water’ stools, containing flakes of mucus, epithelial cells and large numbers of V. cholerae. Abdominal pain and vomiting occur later. Fluid loss can lead to severe dehydration, acidosis, shock and circulatory collapse. Death can occur, and be very rapid (within a few hours), if patients are not rehydrated.
Ingested V. cholerae probably colonise the small intestine by attaching to intestinal epithelial cells, where they proliferate and excrete a potent enterotoxin. Secreted enterotoxin enters intestinal epithelial cells and activates adenylate cyclase. Intracellular cAMP levels increase, while H2O, Na+, K+, Cl− and HCO3– are secreted into the lumen of the small intestine, producing diarrhoea.
The infectious dose is high, around 106 CFU. Typically, water-borne cholera is spread by poor sanitation, producing contaminated water supplies, which can also subsequently produce contaminated filter-feeding shellfish. Seafood, including raw, lightly cooked or recontaminated shellfish or fish, is the most common source of food-borne cholera.
1. Consume only potable water.
2. Dispose of sewage correctly.
3. Use only potable water in seafood harvesting and preparation.
4. Do not harvest seafood from waters containing V. cholerae.
6. Chill seafood to <4°C at harvest and after.
7. Exclude infected individuals from handling food.
Vibrio parahaemolyticus causes enteritis, and like V. cholerae, is an inhabitant of marine environments (see above). Marine animals can carry this organism, and asymptomatic carriage can occur in humans. Characteristics of this pathogen are described above.
The incubation period for V. parahaemolyticus enteritis is typically 12 to 24 h, but ranges from 4 h to 4 days (Anon., 1992f). Symptoms include diarrhoea, cramps, nausea, sometimes vomiting, low fever, chills and headache. The disease is usually self-limiting. Sequelae may include reactive arthritis.
V. parahaemolyticus enteritis is probably an infection with an unknown toxin produced in the GI tract. Invasion probably occurs via blood. They produce a heat-stable haemolysin (Kanagawa factor), which may be involved in pathogenicity, amongst other possible factors. However, toxins can also be formed in food.
The infectious dose is not known, but may be around 104 CFU (or greater for healthy individuals). In Japan, V. parahaemolyticus is the leading cause of food-borne disease, where consumption of raw, contaminated seafood is the major cause. In the USA, most cases occur via cross-contaminated seafood.
1. Do not harvest seafood from contaminated waters.
2. Chill seafood to <4°C at harvest and after.
4. Avoid raw seafoods particularly those harvested from estuaries during summer.
Vibrio vulnificus causes septicaemic invasive infection and, like other Vibrio (see above), occur in marine environments, including seawater and marine sediments.
The incubation period is typically 16 to 38 h, but ranges from 7 h to several days (Anon., 1992g). Symptoms include fever, chills, nausea and hypotension. People with higher than normal iron levels are more susceptible. Necrotic skin lesions appear in most patients, with oedema, tissue necrosis and death frequent. Amputation is often required.
The infectious dose is <102 CFU for susceptible individuals. Raw oysters have caused this food-borne infection, while other seafoods do not normally harbour V. vulnificus. They can cause septicaemia via skin lesions or wounds.
1. People with liver disease or other chronic disease should not eat raw shellfish, particularly oysters.
2. Avoid raw seafoods, particularly those harvested from estuaries during summer.
Yersinia enterocolitica serogroups O3, O5, O8 and O9 cause the invasive infection termed yersiniosis. Y. enterocolitica is very common in the throat, tonsils and faeces of pigs, but is also found in water, soil and dogs. Dogs may be a reservoir for non-food-borne yersiniosis.
Y. enterocolitica are facultatively anaerobic rods, non-motile at 37°C, but usually motile at 30°C (Bercovier and Mollaret, 1984). The pathogen can grow at refrigeration temperature (tmin −2°C) but topt is around 30°C. Grows in 5% NaCl, and survives alkaline pH well (Bercovier and Mollaret, 1984).
The incubation time is typically 24 to 36 h, but may be 3 to 11 days (Anon., 1992h). Symptoms include abdominal pain, fever and diarrhoea; nausea and vomiting are less frequent. Abdominal pain can be severe, and may be mistaken for appendicitis, and enteric symptoms can last for months. Sequelae include reactive arthritis, Reiter’s syndrome and septicaemia. The young, elderly and IC individuals are most at risk.
Y. enterocolitica produce a local inflammatory response after internalization in intestinal epithelial cells. A heat-stable enterotoxin can be produced in vitro, but has not been found in vivo, and its role is unknown.
The infectious dose is not known (Nesbakken, 2000). Foods involved have included putatively pasteurized milk and flavoured milk, water, chow mein and tofu. Pork meats are often implicated as the source of infections (Nesbakken, 2000). However, although pork meats – including tongue and chitterlings (intestines) – frequently contain Y. enterocolitica, these have not yet been proven as vehicles of food-borne yersiniosis.
1. GHP in food production.
3. Use only potable water in food manufacturing; consume only potable water.
5. Prevent cross-contamination of heat-treated foods.
6. GHP when handling domestic pets.
Listeria monocytogenes cause the invasive infection listeriosis, a disease of humans and livestock, although non-invasive disease can also occur in humans (see below). L. monocytogenes can be carried asymptomatically in the GIT of livestock, other animals and humans, and can be shed in the milk of cows with or without mastitis symptoms (Farber and Peterkin, 2000). The pathogen is ubiquitous in the environment, including food processing plants, refrigerators, drains, soil, water, sewage, dust and on plant tissues (Seeliger and Jones, 1986). L. monocytogenes has been found in improperly fermented silage, which is suspected as being a source of listeriosis in livestock.
L. monocytogenes are rods, motile at 25°C, but usually non-motile at 37°C (Seeliger and Jones, 1986). The organism is a facultative anaerobe, but prefers a microaerophilic atmosphere if O2 is present. L. monocytogenes is capable of growth on food at −1.5°C, and can grow in vitro up to 45°C. The pathogen can proliferate at pH 4.1 to 9.6, and in 10% NaCl. L. monocytogenes is very resistant to drying, can form persistent biofilms in food manufacturing plants, and can survive 1 year in 16% NaCl.
Two forms of human listeriosis are recognized, and both are commonly food-borne. Invasive listeriosis symptoms include septicaemia, meningitis, encephalitis and spontaneous abortion (Anon., 1992l). People at high risk of invasive listeriosis are IC individuals (pregnant women, AIDS patients, cancer patients, young, elderly) and those with diabetes, heart or hepatic disease (Farber and Peterkin, 2000). In pregnant women, spontaneous abortion usually occurs in the third trimester, resulting in death of the infant. Non-invasive listeriosis symptoms are mostly enteric and include diarrhoea, mild fever, headache and myalgia, and the disease has a short incubation period (1 to 3 days). Healthy individuals are at risk for noninvasive listeriosis. However, due to its environmental ubiquity, it follows that L. monocytogenes is regularly consumed via foods by healthy people without causing illness.
In invasive listeriosis, L. monocytogenes passes through intestinal epithelia, probably via intestinal epithelial cells or Peyer’s Patches (Farber and Peterkin, 2000). Subsequent spread via the blood and lymphatic systems to the liver and spleen occurs, after which the pathogen is largely killed by macrophages, and cleared from the circulatory system. However, if the immune response in the liver is inadequate, surviving L. monocytogenes proliferate intracellularly within liver macrophages. L. monocytogenes then commences a process of cell-to-cell spread, inducing cell death, and spreading to the CNS, heart, eyes or foetus. In non-invasive listeriosis, the pathogen is probably efficiently cleared from the circulatory system by immune response macrophages.
The infectious dose is not known, but for invasive listeriosis appears low (>100 CFU) for IC individuals, so growth of the pathogen in food is not necessary. Generally, high doses (>105 CFU) of L. monocytogenes appear to be involved in non-invasive listeriosis, so prevention of L. monocytogenes growth in foods is a priority in avoiding this form. Foods that have been proven vehicles of infection include soft cheese, raw and pasteurized milk, ready-to-eat meat products (paté), poultry products (turkey frankfurters), seafood products, vegetables and fresh salads.
1. Use GHP and HACCP in food production.
2. Immunocompromised individuals and other target populations should avoid high-risk foods.
3. Pasteurize milk and dairy products; don’t consume unpasteurized products.
4. Prevent cross-contamination and recontamination of heat-treated foods.
5. Completely separate raw and cooked products during meat product manufacture.
6. Re-heat ready-to-eat foods adequately.
7. Do not use organic waste or faecally contaminated water on ready-to-eat crops.
8. Use the hurdle concept to limit growth of L. monocytogenes in foods.
9. Use correct starter cultures in cheese and meat fermentations.
Staphylococcus aureus causes the food-borne intoxication staphyloenterotoxicosis. S. aureus produces a range of enterotoxins in food (A, B, C1, C2, C3, D, E, F) (Baird-Parker, 2000). Most human food-borne disease is caused by type A enterotoxin (Anon., 1992m). S. aureus is harboured in the anterior nares of up to 50% of people, but is also a common environmental contaminant found in dust, air, water, vegetation and on environmental surfaces (Kloos and Schliefer, 1986). S. aureus primarily causes enteric illness, but also causes skin and throat lesions in man and animals.
S. aureus are non-motile, facultatively anaerobic cocci. Growth occurs at 6.7 to 48°C and at pH 4.0 to 9.8. S. aureus survives desiccation extremely well, tolerates up to 20% NaCl, and can grow in aw of 0.83 (Kloos and Schliefer, 1986). Enterotoxin is not produced below 8°C, but enterotoxin A is produced in 10% NaCl. S. aureus enterotoxins are extremely heat stable and are typically not destroyed by boiling for 30 minutes, so their formation in food must be prevented.
The incubation period is typically 1 to 6 h (Anon., 1992m). Symptoms include nausea, vomiting, abdominal cramps, diarrhoea, sweating, headache and possibly a drop in body temperature. Fluid does not accumulate, but the CNS is stimulated, triggering the emetic centre in the brain, thus inducing vomiting.
Growth of the pathogen in food is necessary, as large numbers of S. aureus (>105 CFU/g per g, but commonly 107 CFU/g) are required to produce enough toxin (<1 μg) in food to cause illness. Poor hygiene amongst food handlers with skin infections, or those who carry the pathogen in their nostrils, is frequently a primary factor in outbreaks of food-borne staphyloenterotoxicosis. Foods that have been proven vehicles of infection include cold, cooked and handled cream- and custard-filled bakery products, custard, cream-based desserts, milk, meat, canned fish, seafood and fermented sausages.
2. People with skin infections should not handle foods.
3. Use GHP when handling foods.
4. Chill cooked food rapidly in small quantities.
5. Store cooked or heat-treated foods at <4°C or >60°C.
6. Avoid extensive handling of foods.
7. Avoid delays between cooking and eating.
Clostridium perfringens causes the toxico-infection perfringens food poisoning. Perfringens food poisoning is most commonly caused by organisms producing type A enterotoxin. Other types of enterotoxin (B to G) do not normally cause food-borne disease (Labbé, 2000). C. perfringens is ubiquitous in the environment, and is frequently detected on spices, raw meats, soil (levels up to 104 CFU/g), water, sewage and dust. Asymptomatic faecal carriage occurs in animals (Cato et al., 1986).
C. perfringens are spore-forming rods which prefer a low redox potential (Eh) environment (usually anaerobic). Spores are resistant to environmental extremes. Growth occurs between 15 and 50°C, with topt between 40 and 45°C, and at pH 5.5 to 8.0. Growth is usually inhibited in 7 to 8% NaCl (Cato et al., 1986). Enterotoxin is produced optimally at 35 to 40°C.
The incubation period is typically 8 to 22 h (Anon., 1992k). Symptoms include severe abdominal pain with profuse diarrhoea. Vomiting, nausea or fever are rare. The young and elderly are more at risk. Infection with type C can cause necrosis and haemorrhage in the small intestine. This type is common in Papua New Guinea, and is rare, but does occur, in other countries.
Ingested vegetative cells sporulate in the small intestine, releasing enterotoxin. Enterotoxin damages the brush border of epithelial cells, disrupting water and ion flux, and producing fluid movement and diarrhoea (Labbé, 2000). The illness may last for up to 2 days, and recovery is usually complete.
The infectious dose is believed to be high, >106 CFU/g, indicating that growth in foods is necessary. Some cases appear to have ingested preformed toxin (probably as well as vegetative cells), which may have induced shorter than normal incubation times. A common chain of events involves contaminated foods, cooked in bulk and inadequately cooled. The cooking procedure activates C. perfringens spores which germinate in the anaerobic conditions. The pathogen proliferates once the dish has cooled to an appropriate temperature, leading to ingestion of large numbers of vegetative cells. Foods involved are meat and poultry dishes, particularly those containing gravy, and those with long, slow cooking. Cooking foods in bulk and in advance is frequently a contributing factor, so perfringens food poisoning is mostly associated with bulk catering.
1. Cook food thoroughly to kill vegetative cells.
2. Chill cooked food, especially meat dishes, rapidly in small quantities.
3. Store cooked food at <5°C or >60°C to prevent growth.
4. Limit the storage interval for cooked food to reduce growth of survivors.
5. Reheat food to at least 75°C to kill vegetative cells and to inactivate toxin if pre-formed in food.
6. Remove soil and dust from food to reduce spore contamination.
Bacillus cereus causes two types of food-borne human disease. Emetic syndrome is an intoxication, while diarrhoeal syndrome is a toxico-infection. B. cereus is a common inhabitant of soil, water, dust, vegetation, spices, dried foods and human faeces.
B. cereus are facultatively anaerobic, spore-forming rods; most strains are motile. Growth occurs between 10 to 50°C, topt is 28 to 35°C. B. cereus grows at pH 4.9 to 9.3 (Claus and Berkeley, 1986). Spores are heat resistant.
The incubation period is quick, typically 1 to 6 h (Anon., 1992i). Symptoms include nausea, vomiting and malaise. Diarrhoea may occur later. The symptoms can appear similar to S. aureus food poisoning. The emetic toxin is very heat- and acid-stable.
The infectious dose is believed to be high, around 108 CFU/g of food, so the pathogen must grow in the food. A frequent chain of events involves contaminated foods, cooked in bulk and inadequately cooled, enabling spores which have survived cooking to germinate and proliferate. Preformed toxin is ingested. Foods which have been involved include fried rice (boiled first, then stored and subsequently flash-fried), boiled rice, potato and pastas. Any foods prepared in bulk and improperly cooled could be a risk.
1. Prepare food in small batches.
2. Chill cooked food rapidly in small quantities.
3. Store cooked food at <5°C or >60°C.
4. Re-heat cooked foods thoroughly to kill vegetative cells.
The incubation period is typically 8 to 16 h. Symptoms include nausea, abdominal pain and watery diarrhoea. Vomiting is rare. Spores or vegetative cells are ingested, and toxin is produced in the GIT.
The infectious dose is usually 105 to 108 CFU/g of food, so faults allow B. cereus growth to occur. Proteinaceous foods, vegetables, sauces and puddings have been implicated.
Measures to control B. cereus diarrhoeal syndrome are the same as for emetic syndrome.
Clostridium botulinum causes two types of food-borne human disease. Botulism is an intoxication, whereas infant botulism (floppy baby syndrome) is a toxico-infection. C. botulinum is an environmental contaminant and is found typically in damp soils and muddy sediments, marine and fresh waters (Lund and Peck, 2000). Asymptomatic carriage occurs in the GIT of animals and humans (Cato et al., 1986).
C. botulinum are spore-forming rods which proliferate in low Eh environments (usually anaerobic). The spores are resistant to environmental extremes, but spores may germinate even if oxygen is present (Lund and Peck, 2000). Conditions for growth and toxin production are very strain-dependent. Some strains grow at 3°C, others as high as 48°C (Cato et al., 1986). C. botulinum grows in 5% NaCl, but not in 10% salt or below pH 4.6. Nitrite and competitive microorganisms on foods are inhibitory. The toxin is heat labile, so can be destroyed by heating.
Ingestion of C. botulinum toxin types A, B, E and F is the usual cause of food-borne botulism, although four other toxin types are known and have occasionally been involved (Anon., 1992j; Lund and Peck, 2000). The incubation period is typically 12 to 36 h, but ranges up to 8 days, and probably depends on the level of toxin ingested. Botulinum toxin is very potent: it is estimated that only 0.1 to 1.0 μg can cause food-borne disease (Anon., 1992j). Symptoms include nausea and vomiting followed by dizziness, difficulty swallowing, slurred speech, blurred vision and headache. Fatigue, muscle weakness, paralysis and respiratory impairment can occur. Respiratory failure can cause death (the mortality rate is 30 to 60% in hospitalized individuals).
Botulinum toxin is absorbed into the body by unknown means, attaches to neuromuscular junctions, becomes internalized, and prevents release of acetylcholine. Prognosis is normally improved by rapid administration of antitoxin (Lund and Peck, 2000).
As toxin must be pre-formed in food, growth of the pathogen in food is necessary. This mostly occurs in anaerobic environments, so in Western countries, home-canned, and sometimes commercially canned, non-acid foods (fish, shellfish, meats, vegetables, fungi) are the most common source of botulism. Growth of the pathogen in canned foods is not necessarily evident, as off-odours or can-blowing do not always occur. Other proven sources of botulism include chopped garlic in oil, hazelnut purée, sausages and fish eggs. Fermented fish products and bean products, in Japan and China, respectively, are more frequent sources than other foods. Sea mammal products are common sources of infection in Inuit populations.
1. Avoid home canning of vegetables, fish and meats.
2. Discard cans with faulty seals.
3. Heat any suspect food to 80°C for 15 minutes to destroy toxin.
4. Store home-canned foods at <3°C.
5. Use the hurdle concept for home canning of food.
Infant botulism produces neuromuscular symptoms similar to botulism, resulting in constipation, weak cry and respiratory distress. Infant botulism is usually mild, but depends on the individual patient. Children under 1 year old do not have established gut microflora, so the pathogen may colonize more easily than in other individuals. Infant botulism has occurred in adults, when it has been associated with abnormal GIT function (Lund and Peck, 2000).
The organism is ingested and proliferates in the GIT, producing toxin. Honey is the most common source, and batches from outbreaks have contained up to 104 spores/kg (Lund and Peck, 2000). Powdered formula milk caused one case in the UK, in July 2001. Theoretically, any foods that are not heat treated could be a vehicle of infection.
1. Do not feed honey to babies or infants.
2. Do not feed infants non-heat treated foods.
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Anon. (2000b) Notifiable diseases on-line. Public Health Agency of Canada, dsol-smed.hc-sc.gc.ca/dsol-smed/ndis/index_e.html (accessed 2 November 2004).
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Anon. (2003b) Swiss zoonoses report 2003; Salmonella, Campylobacter, STEC, Listeria. FVO-magazine Information Service, www.biret.admin.ch/info-service/e/publikationen/magazin/1_index.html (accessed 28 October 2004).
Anon. (2004a) Annual report on zoonoses in Denmark 2003. Ministry of Food, Agriculture and Fisheries, www.dfvf.dk/files/filer/zoonosecentret/publikationer/annual%20report/annual_report_2003-endelig.pdf (accessed 28 October 2004).
Anon. (2004b) Incidence of cases of infection with nine pathogens under surveillance by the Foodborne Diseases Active Surveillance Network, by site, compared with national health objectives for 2010 – United States, 1996, 1998 and 2003. Centers for Disease Control and Prevention, www.cdc.gov/mmwr/preview/mmwrhtml.mm5316a2.htm#tab (accessed 28 October 2004).
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Beery, J.T., Hugdahl, M.B. and Doyle, M.P. (1988) Colonization of gastrointestinal tract of chicks by Campylobacter jejuni. Applied and Environmental Microbiology 54, 2365–2370.
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Most food-borne viral diseases are caused by consumption of molluscan shellfish. During filter-feeding of seawater, molluscs concentrate viral particles, originating from human faeces, in their tissues. Many viruses are host-specific, so do not cause disease in both humans and animals. Methods for detection of viruses in foods are generally lacking, although routine PCR-based methods may be developed in the future. DNA or RNA sequence-based typing methods are used, but are not suitable for routine use. The only virus for which standard methods for its detection in foods have been developed is Norovirus in shellfish. Contamination of other foods, which have been implicated in outbreaks of food-borne viral disease, probably occurs via faeces or vomit from infected food handlers either directly or in aerosols, or via faecally contaminated water.
Norovirus (family Caliciviridae) are a group of related, ssRNA viruses. Norovirus were previously described as Norwalk virus (the prototype), Norwalk-like viruses (NLV), Small Round Structured Viruses (SRSV) or calicivirus. Norovirus cause viral gastroenteritis, believed to be a very common cause of enteritis worldwide. Other members of Caliciviridae include Sapovirus – which can cause enteric symptoms in young children, Vesivirus and Lagovirus.
Norovirus are normally transmitted person-to-person by the faecal–oral route, but may also be water-borne. However, it has been detected in shellfish implicated in outbreaks, particularly oysters, clams and shrimps.
The incubation period is typically 1 to 3 days. Symptoms include nausea, projectile vomiting, diarrhoea (watery, voluminous) and abdominal pain. The disease is normally self-limiting. Elderly and IC individuals are most at risk.
Norovirus replicates in the mucosa of the small intestine and is shed in large numbers in faeces.
The infectious dose is not known. Any foods that require extensive handling could be vehicles of infection. Foods most commonly involved are shellfish, but fruits and salads have also been associated with infection.
1. Don’t consume raw shellfish.
2. Prevent faecal contamination of food, even pre-harvest.
3. Dispose of sewage in a sanitary manner.
4. Infected individuals should not handle food.
5. Prevent cross-contamination from shellfish to other foods.
Hepatitis A virus (HAV) is a ssRNA virus of the family Picornaviridae.
The incubation period is typically 2 to 9 weeks, so food may become contaminated with HAV before the onset of symptoms, but after faecal shedding has commenced. Early symptoms are anorexia, fever, malaise, nausea and abdominal discomfort. Vomiting and fever can occur. Sequelae include liver damage, seen in patients when jaundice develops. Hepatitis E virus (HEV) causes similar human disease, but belongs to the family Hepeviridae. While HEV has potential to be food-borne it is believed to have caused water-borne disease.
HAV is absorbed through the gastrointestinal mucosa and carried via the blood to the liver. HAV then binds to receptor sites on the hepatocyte surface and penetrates cells. Viral replication occurs, HAV is excreted in bile, and shed in faeces.
Food-borne transmission appears to have occurred in some HAV outbreaks, but the virus has not been detected in any foods. The long incubation period frequently means suspect foods are unavailable, and in-food detection methods have not been developed. HAV is transmitted person-to-person by the faecal–oral route. The infectious dose is unknown but likely to be low: perhaps ten to 100 virus particles. Implicated foods include water, shellfish, salads, fruits, cold meats, sandwiches, fruit juices, milk, milk products and iced drinks.
1. Prevent faecal contamination of food even pre-harvest.
2. Infected individuals should not handle food.
4. Prevent overcrowded living conditions.
5. Use good personal hygiene measures.
Rotavirus is a dsRNA virus, of the family Reoviridae. Rotavirus is transmitted person-to-person by the faecal–oral route, and causes viral gastroenteritis. Believed to have only rarely caused food-borne disease, but may be more commonly water-borne. Rotavirus has not been isolated from foods.
Rotavirus is the most common cause of viral gastroenteritis in children < 2 years old, and most or all children contract this virus after birth.
The incubation period is typically 1 to 3 days, and vomiting can last from 4 to 8 days after symptoms commence. Symptoms include vomiting, watery diarrhoea and low-grade fever. Rotavirus is normally self-limiting but, in severe cases, rehydration of patients is necessary.
Rotavirus replicates in the mucosa of the jejunum or ileum and is shed in faeces in large numbers.
The infectious dose is unknown but probably is ten to 100 virus particles. Water is most commonly implicated, but any foods that require extensive handling could be vehicles of infection. Implicated foods include salad, cold foods, shepherd’s pie and school lunches. Poor personal hygiene is frequently a contributing factor.
1. Infected individuals should not handle food.
3. Prevent faecal contamination of food.
Chemicals can occur in the food chain due either to their existence in the environment through unintentional contamination of food, or to their intentional use somewhere along the food production chain (Table 1.2). Generally, industrial pollutants are unintentional contaminants of foods, so, even if regulated, may be difficult to control. Agricultural chemicals are deliberately applied to land or crops during production, so their use can be both regulated and controlled. Some toxic chemical compounds can occur naturally in foods and in the environment.
The rate of ingestion of chemical hazards by food animals can be either higher or lower than the rate of their excretion. In the former case, accumulation of chemicals occurs. In the latter case, animals have a ‘decontaminating’ effect from the public health perspective. Hazards that accumulate can be a greater public health risk than those which do not accumulate, because if animals are exposed even only to low levels of accumulating hazards but over extended time, their tissues can finally contain levels that pose a risk to consumers. With chemical hazards that accumulate, older animals are a higher risk than younger animals.
Heavy metals which can occur in foods include lead, arsenic, mercury, cadmium, copper, fluorine and selenium.
Lead can occur in animals grazing close to lead-smelting plants or after ingestion of paints or lead-containing substances. Paint (typically older types of paint) on animal housing and fences may contain lead and be licked/chewed by farm animals. Animals accumulate lead in the bones, and acute exposure results in high lead levels in the liver and kidney. After chronic poisoning, softening and cavitation of the CNS can be found.
Food animal exposure typically occurs via feeds or liquids contaminated with arsenical herbicides, rodenticides or insecticides. Arsenical compounds have been used as antiparasitics in the past, but are now largely obsolete. Accumulation of arsenic occurs in the liver and kidney, when fatty degeneration can be seen. Arsenic also accumulates in the bones of animals.
Table 1.2. Main groups and typical examples of chemical hazards in foods.

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