Foodborne viral infectionsBMJ 1999; 318 doi: https://doi.org/10.1136/bmj.318.7196.1433 (Published 29 May 1999) Cite this as: BMJ 1999;318:1433
Most are caused by Norwalk-like viruses, but we need to know more about these
- Antony Hale (), Senior registrar in virology
Media attention on outbreaks of infection caused by salmonella species and Escherichia coli 0157 and more recently on new variant Creutzfeldt-Jakob disease have highlighted the importance of foodborne transmission of infectious agents, but what of the role of viruses? A recent report from the Advisory Committee on the Microbiological Safety of Food (ACMSF) provides a timely reminder of the importance of these agents, points to gaps in our knowledge, and offers advice for their control.1
Although the list of viruses causing intestinal disease in humans is long, the epidemiology of foodborne outbreaks in the United Kingdom reveals the predominance of a single group, the Norwalk-like viruses.2 Also known as small round structured viruses, these are an antigenically diverse group of caliciviruses which have similar morphology under the electron microscope and appear to cause an identical clinical picture of projectile vomiting and diarrhoea. They include Hawaii, Snow Mountain, Taunton, Mexico, and Grimsby viruses.3 4
Norwalk-like viruses can cause illness at any age, possibly due to their antigenic diversity but also because infection appears to induce only short term immunity.5 Although other enteric viruses such as rotaviruses, astroviruses, and Sapporo-like viruses (caliciviruses which are morphologically and genetically distinct from Norwalk-like viruses) have also been associated with foodborne outbreaks, most of us are protected by long term immunity acquired during childhood. Hepatitis A virus is a rare cause of foodborne outbreaks in the United Kingdom but is noteworthy because the level of immunity to this virus is falling in the population and infection can be life threatening. Indeed, a recent report from Finland of two outbreaks of hepatitis A virus infection linked to centrally prepared food emphasises the potential risks posed by this virus.6
There appear to be two important means of transmission of viruses to food. The first is the contamination of bivalve shellfish harvested from inshore coastal waters. In filtering large volumes of seawater during feeding the shellfish sequester viruses.7 Although depuration reduces the load of pathogenic bacteria, it does little to remove viruses.8 These viruses will be inactivated during cooking, but shellfish that are not sufficiently cooked or eaten raw present risks. One such shellfish, the oyster, is usually preferred uncooked and consequently causes most outbreaks of viral infection associated with shellfish. The second, numerically more important route of transmission, is the contamination of food during preparation by infected food handlers. Any type of food may be contaminated by this means, although more frequently handled foodstuffs, such as salads, are more commonly implicated as a vehicle of transmission. Breakdown in good hygienic practice is the cause of these incidents. Food workers with infection with Norwalk-like viruses should not be handling food until 48 hours after becoming symptom free. The situation is not so straightforward for hepatitis A infections as individuals are infectious before the onset of symptoms.
At first glance viruses appear to be an uncommon cause of fooborne infection. An analysis of outbreaks of infectious intestinal disease reported to the Communicable Disease Surveillance Centre in 1995-6 showed Norwalk-like viruses to be associated with only 6% of foodborne outbreaks, whereas these viruses caused 60% of outbreaks of gastroenteritis, where the mode of transmission was mainly from person to person.9 Pathogenic bacteria and toxins were more commonly associated with foodborne outbreaks, although no agent was identified in 12% of incidents. However, the available data are limited and probably seriously underestimate the importance of foodborne virus infections.
Norwalk-like viruses are difficult to detect.10 Electron microscopy of faecal specimens has been the mainstay of diagnosis in the United Kingdom, but virus is shed in relatively small numbers and only for a short time after the onset of symptoms. Until very recently it has been impossible to identify Norwalk-like viruses in contaminated food as these viruses do not grow in tissue culture. In addition, reported outbreaks of Norwalk-like virus infections are likely to represent only a small proportion of community acquired Norwalk-like virus infections. Much less is known about the burden of sporadic Norwalk-like virus disease, in particular the proportion due to foodborne transmission. We should soon have an answer to this important question when a government commissioned study of intestinal infectious disease in the community is published. Thus, although Norwalk-like viruses are not likely to be as important as enteropathogenic bacteria as a cause of foodborne illness, the total number of people affected each year is probably high.
The report of the Advisory Committee on the Microbiological Safety of Food clearly lays out the many problems in assessing and controlling foodborne viral infections and makes 17 recommendations which fall into four broad areas. These are: (a) improved surveillance and diagnosis of foodborne outbreaks; (b) a reduction in environmental contamination with sewage, particularly of shellfish harvesting areas; (c) increased investment into the use of new molecular methods for identifying Norwalk-like viruses in food and for assessing measures for viral inactivation; and (d) an improvement in hygiene in the food industry, an important point which cannot be overstated.11 These measures are to be welcomed as they will improve our understanding of the importance of these agents and, if implemented fully, should lead not only to a reduction in foodborne viral illness but also to an overall reduction in foodborne disease.