SHERYL AVERY

There are three categories of microbial food-borne diseases:

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

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.

Measures to control campylobacteriosis include:

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

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.

Measures to control salmonellosis include:

1. Cook foods thoroughly.

2. Pasteurize milk and dairy products; avoid consumption of unpasteurized products.

3. Prevent cross-contamination of heat-treated foods.

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.

Typhoid fever and paratyphoid fever

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.

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.

Measures to control typhoid and paratyphoid fevers include:

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.

5. Cook food thoroughly.

6. Prevent cross-contamination of heat-treated foods.

7. Exclude infected or carrier-status individuals from handling food.

8. Give antibiotic therapy to prevent long-term carrier status developing.

Escherichia coli O157

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).

Measures to control E. coli O157 include:

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

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.

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.

Measures to control shigellosis include:

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

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 t_min 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 pH_opt of 7.8 to 8.6. Vibrio are sensitive to heat: cooking to 65°C kills this pathogen.

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.

Measures to control cholera include:

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.

5. Avoid raw seafoods.

6. Chill seafood to <4°C at harvest and after.

7. Exclude infected individuals from handling food.

Vibrio parahaemolyticus

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.

3. Prevent cross-contamination.

4. Avoid raw seafoods particularly those harvested from estuaries during summer.

Vibrio vulnificus

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.

Measures to control V. vulnificus food-borne septicaemia include:

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

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 (t_min −2°C) but t_opt 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.

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.

Measures to control yersiniosis include:

1. GHP in food production.

2. Pasteurize milk and dairy products; don’t consume unpasteurized products.

3. Use only potable water in food manufacturing; consume only potable water.

4. Cook meats thoroughly.

5. Prevent cross-contamination of heat-treated foods.

6. GHP when handling domestic pets.

Gram-positive Bacterial Pathogens

Listeria monocytogenes

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.

Listeriosis

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.

Measures to control listeriosis include:

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 a_w 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.

Measures to control staphyloenterotoxicosis include:

1. Use good personal hygiene practices when handling foods.

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

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 t_opt 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.

Measures to control perfringens food poisoning include:

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

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 emetic (vomiting) syndrome

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.

Measures to control B. cereus emetic syndrome include:

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.

B. cereus diarrhoeal syndrome

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

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).

Botulism

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.

Measures to control botulism include:

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

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.

Measures to control infant botulism include:

1. Do not feed honey to babies or infants.

2. Do not feed infants non-heat treated foods.

References

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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.

Noroviruses

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.

Measures to control Norovirus include:

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.

Measures to control HAV include:

1. Prevent faecal contamination of food even pre-harvest.

2. Infected individuals should not handle food.

3. Dispose of sewage in a sanitary manner.

4. Prevent overcrowded living conditions.

5. Use good personal hygiene measures.

Rotavirus

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.

Measures to control rotavirus include:

1. Infected individuals should not handle food.

2. Dispose of sewage in a sanitary manner.

3. Prevent faecal contamination of food.