Viruses are now recognized as a leading cause of food- and waterborne disease. For many non-bacterial gastroenteritis outbreaks, a viral etiology is now being indicated in the laboratory. One such virus, Norwalk, was the leading cause of foodborne disease in the U.S. in 1982, with 5000 cases occurring in two large outbreaks.
The most important viral food- and waterborne diseases have been poliomyelitis, infectious hepatitis and viral gastroenteritis. The first two are sufficiently distinct clinically to permit diagnosis without isolation of the agent. Poliomyelitis (due to poliovirus, an enterovirus) was first reported to be transmitted via food in 1914. Eighteen food- or waterborne outbreaks were reported (U.S., U.K., Sweden, one in Canada) to 1949, with none since. Another enterovirus, echovirus 4, was responsible for a single outbreak of illness in the U.S. (1976), in 80 picnickers, with the suspected vehicle being coleslaw.
There have been over 300 food- and waterborne outbreaks of hepatitis recorded worldwide since 1895, attributed to hepatitis A virus. The major vehicles have been contaminated water and shellfish, with the largest outbreak involving 292,301 persons in China in 1988, due to the consumption of cockles. There have been nine documented outbreaks of food- or waterborne hepatitis in Canada. A few outbreaks of hepatitis due to a non-A, non-B hepatitis virus have been recorded worldwide, all associated with water; two were in North America (Mexico, 1986).
Gastroenteritis viruses which may cause food- or waterborne disease include Norwalk and Norwalk-like viruses, fecal parvoviruses, rotaviruses, enteric adenoviruses 40 and 41, astroviruses, caliciviruses and coronaviruses. All of these are spread by the fecal-oral route. Only the first three types have definitely been linked to food- or waterborne illness. The Norwalk agents predominate in North America through vehicles which include water (for drinking or swimming), shellfish, and a variety of other foods, many contaminated by ill food handlers. At least one foodborne outbreak attributed to Norwalk virus occurred in Canada (Winnipeg, 1987); pastries served in a hotel by ill food handlers affected 47 persons. Several other Canadian food- or waterborne non-bacterial outbreaks with a Norwalk virus pattern of illness have been reported. However, only in some of these outbreaks was Norwalk-like virus actually observed in the stools of affected persons. Studies in the U.S. indicate that the presence of antibody against Norwalk virus does not prevent reinfection and this phenomenon may account for the high incidence of this virus.
Although detection of virus in foods by laboratory methods is desirable in an outbreak situation, in many cases it is difficult or impossible. Polioviruses and many of the enteroviruses infect and grow in cell cultures and can be identified with specific-antibodies. In theory, a single infectious particle can be detected in a susceptible cell culture. To prepare food samples for inoculation into cell cultures, virus is extracted into a nontoxic fluid and may require concentration (as for water samples) by methods such as ultracentrifugation, ultrafiltration or organic flocculation. Although some strains of hepatitis A virus and rotavirus have been adapted to grow in cell culture, wild strains generally do not. Some viral antigens, however, may be produced in cell culture and be detectable as foci using fluorescein- or enzyme-labelled antibody. Non-A, non-B hepatitis virus, the Norwalk type viruses and parvoviruses are not known to infect cell cultures. Their detection depends on enzyme-linked immunoassay or immune electron microscopy, methods which require at least 106 viral particles per ml and supplies of specific antisera, which are not widely available. Numerous enzyme linked immunoassay and agglutination kits are available commercially for rotavirus detection; but these tests are not sensitive enough for use in foods where the virus quantities are normally low. DNA and RNA probes for hepatitis A virus have been developed and may prove useful for detection in foods.
The characteristics of hepatitis and gastroenteritis diseases and their agents, transmitted via food or water, are presented in tabular form. A fact sheet
Table 1.
Food- and waterborne diseases.
| Disease (other names) | Virus and source | Characteristics of virus | Target population | Incubation period | Symptoms | Duration of illness | Mortality |
|---|---|---|---|---|---|---|---|
| Hepatitis A (hepatitis, infectious hepatitis, viral hepatitis) | Hepatitis A virus, classed as enterovirus 72, present in stools of infected persons | Featureless, 27–32 nm, icosahedral in shape, single-stranded RNA, only one serotype known | All age groups are susceptible if not immune due to previous exposure, young adults have the highest rates | 10–50 (28) days | Vary from inapparent to severe with jaundice, symptoms prior to jaundice — nausea, vomiting, fever, dark urine, abdominal pain, malaise, anorexia | 1–2 weeks if mild, months if severe, virus shed in feces up to 14 days prior to symptoms and at lower levels for 7–10 days after | Low, about 0.1% of those infected, 0.5% of those with jaundice |
| Non-A non-B hepatitis (hepatitis, infectious hepatitis, viral hepatitis) | Non-A, non-B hepatitis virus, unclassified at present, present in stools of infected persons | About 27 nm in diameter | All age groups are susceptible if not immune due to previous exposure | 14–120 (40) days | As above | As above | Probably less than 0.5% of those infected |
| Norwalk and Norwalk-like gastroenteritis (non-bacterial gastroenteritis, viral gastroen-teritis, winter vomiting disease) | Norwalk virus and Norwalk-like viruses (Snow Mountain, Hawaii, Montgomery County, Amulree, Taunton, Otofuke, Sapporo), present in stools of infected persons | Small, round, structured, 27–32 nm, of undetermined nucleic acid, several serotypes exist | All age groups, highest incidence in adolescents and adults | 12–48 (36) hours | Vomiting, diarrhea, malaise, fever, nausea, abdominal cramps | Usually 1–3 days, virus excreted while symptomatic and longer in some cases | Usually low can be fatal in the infant, elderly, or debilitated patient |
Table 1A.
| Disease | Minimum infectious dose | Foods associated with outbreaks | Factors contributing to foodborne illness | Control measures | Criteria for confirming an outbreak |
|---|---|---|---|---|---|
| Hepatitis A | Probably low, 10–100 virus particles | Fecal-contaminated water and shellfish, other foods via ill food handlers or contaminated water used for cleaning or irrigation | Eating raw or insufficiently cooked shellfish, infected persons preparing or serving food, drinking fecal-contaminated water | Monitor shellfish harvest areas for fecal contamination, consumption of raw shellfish should be discouraged, cook shellfish well, monitor drinking water for fecal contamination, good personal hygiene of food handlers | Demonstration of liver dysfunction (high enzyme levels), presence of IgM-specific antibody, a 4-fold rise in specific antibody in paired serum samples |
| Non-A, non-B hepatitis | As above | Fecal-contaminated water | Drinking fecal contaminated water | Monitor drinking water for fecal contamination | Suspected if screening rules out other known hepatitis agents |
| Norwalk or Norwalk-like gastroenteritis | Presumed to be low, 1 virus particle may infect | Fecal-contaminated water and shelfish, other foods via ill food handlers | Eating raw or insufficiently cooked shellfish, infected persons preparing or serving food, drinking fecal-contaminated water | Monitor shellfish harvest areas for fecal contamination, consumption of raw shellfish should be discouraged, cook shellfish well, monitor drinking water for fecal contamination, good personal hygiene of food handlers | Identification of virus in feces by immunoassay methods or immune electron microscopy, a 4-fold rise in specific antibody in paired serum samples |
Table 2.
Food- and waterborne diseases.
| Disease (other names) | Virus and source | Characteristics of virus | Target population | Incubation period | Symptoms | Duration of illness | Mortality |
|---|---|---|---|---|---|---|---|
| Parvovirus gastroenteritis (non-bacterial gastroenteritis, viral gastro-enteritis, winter vomiting disease | Fecal parvoviruses (Cockle, Wollan, Ditchling, Parramata), present in stools of infected persons | Small, round, featureless, 23–26 nm in diameter with single-stranded DNA, some are immunologically distinct | All age groups | 1–2 days | Vomiting, diarrhea malaise, fever, nausea, abdominal cramps | Usually 1–3 days, virus may be excreted for several weeks after symptoms subside | Probably low |
| Rotavirus gastroenteritis (non-bacterial gastro-enteritis, viral gastroenteritis) | Rotaviruses, present in stools of infected persons | About 70 nm in diameter, double-capsid structure, wheel-like in appearance, double-stranded RNA, several sero-types exist | All age groups, highest incidence in children | 1–3 days | Vomiting, diarrhea myalgia, headache, fever, cramps, nausea, dehydration | 4–10 days | Low |
Table 2A.
| Disease | Minimum infectious dose | Foods associated with outbreaks | Factors contributing to foodborne illness | Control measures | Criteria for confirming an outbreak |
|---|---|---|---|---|---|
| Parvovirus gastroenteritis | Presumed to be low | Fecal-contaminated shellfish | Eating raw or insufficiently cooked shellfish | Monitor shellfish harvest areasfor fecal contamination | Identification of virus in feces by immunoassay methods or immune electron microscopy, a 4-fold rise in specific antibody in paired serum samples |
| Rotavirus gastroenteritis | 50% infective dose = about 10 virus particles, 25% infective dose = 1 particle | Fecal-contaminated water, other foods via ill food handlers | Drinking fecal-contaminated water, infected persons preparing or serving food | Monitor drinking water for fecal contamination, good personal hygiene of food handlers | Identification of the virus in feces by immunoassay, presence of IgM-specific antibody, a 4-fold rise in antibody in paired serum samples |
summarizes pertinent information regarding virus transmission via food.
Fact Sheet on Viruses
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Now recognized as leading causes of foodborne disease.
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Potential to cause large outbreaks of foodborne illness.
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—Humans can become ill mainly by:
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(1)drinking polluted water;
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(2)consuming raw or insufficiently cooked shellfish taken from polluted waters;
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(3)consuming food contaminated by an ill food handler.
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(1)
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Viruses are shed in the feces of infected humans and contaminate foods via sewage or by direct mishandling.
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Viruses are inert, and thus cannot multiply outside a living host cell i.e. they cannot grow in food.
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Viruses are too small to be seen with the light microscope. Most food-borne viruses are spherical and range in diameter from 27 to 70 nm.
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Viruses are made up of nucleic acid (either DNA or RNA) and protein.
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There is a specific “lock and key” relationship between a virus and the host cell it infects. Viruses of nonhuman origin will seldom be able to cause disease in humans.
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Pasteurization of foods will inactivate small amounts of most viruses but a study has shown that 0.1% of hepatitis A virus survived in milk heated at 62.8°C for 30 min. Shellfish tissue is known to protect viruses against heat inactivation.
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UV light and strong oxidizing agents can inactivate viruses present on exposed surfaces or in water.
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Viruses are very resistant to gamma irradiation.
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—Present methods of detection:
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(1)Infection of cell cultures
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(2)Electron microscopy
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(3)Enzyme-antibody assays
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(4)DNA or RNA probe methods
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(1)