Key points are not available for this paper at this time.
Enterically infecting viruses are ubiquitous agents, mostly inducing silent infections. Several are however associated with significant diseases in man from diarrhoea and vomiting to hepatitis and meningitis. These viruses are drawn from a variety of virus families and have different structures and genetic material, yet all are suited to this means of transmission: Normally they are shed in high numbers (assisting environmental transit) and exhibit great particle stability (permitting survival both outside the body and on passage through the stomach). Human activities particularly associated with food and water processing and distribution have the capacity to influence the epidemiology of these viruses. This review provides a description of viruses spreading by these means, their significance as pathogens and considers their behavior in these human-assisted processes. The term virus stems from the Latin virus meaning ‘poison’, and in some ways virus contamination of food resembles toxic contamination more than contamination with other micro-organisms. Viruses are not free living; they are dormant between hosts and have an absolute requirement for living cells in which to replicate. Human viruses require human cells in which to replicate, these are not present in our food and thus such viruses cannot increase in number during storage. The amount of any contaminating viruses should actually decline during storage, and this can be assisted by treatment with chemicals, heat or irradiation. Human viruses do not cause food spoilage and contamination may provide no visible clues to its presence. These features mean that measures to control bacteria will not necessarily control viruses and could actually preserve them. Food-borne viruses are infectious at very low doses and could be introduced at any point in the food chain. Many are difficult (or currently impossible) to culture and detection is no simple task. Outbreaks and sporadic occurrences of food-borne virus infection continue throughout the world. There are simply too many to mention and there is no complete data set. It seems likely that the documented outbreaks are limited only by our ability to document them. The cost of these events is likely to be phenomenal to the community; a single food-borne outbreak of hepatitis A virus (HAV) exposed up to 5000 persons in Colorado. In this case the costs for medical treatment of those infected amounted to approx. 50 000 whilst the cost of tracing and controlling this single outbreak cost over half a million US (Dalton et al. 1996). The burden of infectious intestinal disease (IID) in its broader sense is likewise huge, in the UK the cost per case of norovirus (NoV) -induced gastroenteritis involving a GP visit is estimated at £176 and two persons in every 1000 will make such a visit each year (FSA 2000). The interested reader is referred to several recent reviews (Lees 2000; Seymour and Appleton 2001; Sair et al. 2002; Koopmans and Duizer 2004). As enteric viruses cannot replicate outside their hosts, all such virus transmission is in effect person-to-person. Environmental transit time between hosts may be brief or prolonged. Long-distance travel may take place, e. g. through water systems or even the air. Long-distance travel is accompanied by exposure to the environment and dilution; thus viruses having prolonged environmental transit times must be very stable to survive and are (usually) shed in very large numbers. Enteric viruses meet both requirements; they are acid stable and replicate to prodigious titres in the gut before being shed in concentrated doses directly into the sewage system. All potentially food-borne viruses can also be transmitted directly from person to person via faecal contamination of the environment and viewed in this way food is simply another kind of fomite in environmental transmission, it occupies a special niche simply because of its privileged position in terms of its introduction to the body and the potential it may offer for widespread distribution through trade and commerce. The relative importance of food-borne vs more direct person-to-person transmission is unclear; enteric infections are ubiquitous, single occurrences are far too numerous to mention and statistics usually record only outbreaks (when several people are infected in one location or through one common vehicle). However any one outbreak may involve different types of spread; these viruses have a high secondary attack rate and person-to-person transmission will probably follow even if the virus was actually introduced to that setting by food. This can potentially mask food-borne introductions and it is likely therefore that food-borne transmission is underestimated. There are two types of enterically infecting virus – the first are capable of spreading elsewhere in the body. Infection by these viruses is often subclinical but they may induce signs and symptoms of disease in nonintestinal tissues. These viruses include enteroviruses (e. g. polio or Coxsackie, which may spread to the meninges, central nervous system; skeletal/heart muscle or pancreas) and hepatitis viruses A and E spreading to the liver. The second type of virus are true gut inhabitants. These replicate in the enteric tract, specific symptoms when they occur, are those of a gastrointestinal infection; usually diarrhoea and vomiting but the extent of each component is variable. Table 1 lists the main viruses associated with enteric infection and summarizes their key properties. The most important are illustrated in Fig. 1. Enteric viruses are drawn from a variety of virus families, they range approximately 10-fold in diameter and 20-fold in terms of genome size and complexity. The major enterically transmitted and thus potentially food/waterborne agents comprise (alphabetically) the human adenoviruses (AdV), astroviruses (HAstV), caliciviruses, hepatitis E virus (HEV), parvoviruses, picornaviruses including enteroviruses, kobuviruses and hepatitis A (HAV), and the rotaviruses (RV). Most enteric viruses are childhood infections; spreading largely person-to-person and assisted by the lower hygiene levels in this group. Food-borne transmission may be negligible (AdV) or insignificant (RV) in the developed world. However in the undeveloped world spread of these agents by these routes is poorly characterized. Childhood infection leaves residual immunity that may prevent (or mollify) infection over the rest of an individual's lifetime. Although this is not universally true, in general viruses causing childhood illness are not significant pathogens in healthy adults previously exposed as children. The IID survey in England (FSA 2000) estimated the incidence of GP consultations for intestinal disease by patient age and causative organism. Data from this survey have been reanalysed (Fig. 2) to show the proportion of consultations made for each virus in the age groups 5 years. As expected GP consultations induced by these viruses were biased towards children 5 years (Fig. 2). Infection is particularly common in such as and Incubation is between 24–48 h and illness is usually and with diarrhoea However in those cases when SaV have been to infect adults then symptoms are very similar to those of NoV 1989). hepatitis has been and its infectious was in the middle However the causative agent was identified only in 1972 when the developed of immune electron microscopy the particles to be identified (Kapikian et al. 1972). named to it from hepatitis this agent was found to be for the of infectious were mainly in older children and adults but infection was common in children although in these it to be was found to be a of the family (see and was in the However it some in to its genetic and and it was subsequently to a new of which it is the only can be cultured in cells but this is and for Although for most enterically transmitted hepatitis in the developed it was could account for all enterically transmitted hepatitis in the undeveloped world. Thus the of enterically transmitted hepatitis up. This in was in when a new was identified by means et al. reviewed The genetic organization and particle of the Caliciviruses and was in this However the of the genomic organization and the are such that it could not remain in this it now the only of a group the et al. 2000). is rare in the developed world with cases generally limited to are poorly characterized as agents of enteric infection. is on electron Although associated clearly with gut infection in (e. g. the only infectious human characterized to date is a agent causing a in children. have been associated with gastroenteritis in and secondary in the UK and and et al. et al. Appleton 2001). The agent was identified following a large outbreak in England (Appleton and and was associated with of There is a that of these viruses may actually be caliciviruses (Willcocks et al. infecting the gut were all in the have a appearance under the electron microscope and include the and Most grow well in such as or Formerly the of has polio and the to this virus for this were thought not to be usually associated with diarrhoeal symptoms in but this changed in when was as the agent for an outbreak of gastroenteritis et al. could be in cells and study showed that it had a genome organization of the picornaviruses et al. However the particle in from other picornaviruses and surface projections similar to those of These viruses have now been as a new in the family the are large viruses to the family particles are and may be into the are visible and in the EM the of the can appear the of a from which the virus is named a Illness after an incubation period of d and usually as diarrhoea and vomiting lasting approx. 7 Viruses are shed in high numbers over per of and is a simple Virus is detected by direct by EM or et al. or ELISA account for some million cases of diarrhoea in the US to of hospital admissions for diarrhoea et al. children each year in the US from this virus and in the undeveloped world may amount to et al. 2003). occur in groups but only groups infect humans. A is by far the most common with sporadic to group group is limited largely to Only group A viruses can be these are in each group are into serotypes on their group A there are types of and approx. of This great infections which may be The age for illness is between 6 months and 2 by 4 years most persons have been infected. to is thus exposure to immunity and of illness with age. secondary can occur in for and this provides another means for the virus to spread in the were the most commonly identified enteric in children years in England and and comprised of the virus identification made in this study (FSA 2000). Only of GP consultations for were made by persons >5 years. However this two first not all adult infections are and this small percentage may actually a number of adult GP consultations for infection than for NoV (FSA 2000). viruses replicate and the the upper third of the intestinal cells do not virus of cells the of water from the gut and diarrhoea The in to and the surface for the same time the cells and the with as yet These cells are to virus infection but cannot the of those that have been they require time to Thus until the cells can the This in the is central to in viruses do not attack the cells such infections do occur (e. g. they in diarrhoea from which may not be possible in a young Although most viruses do not some are and induce the of a that can induce diarrhoea if et al. 1996). has no to et al. 1995). It via a it has no effect on and is of the The mechanism of et al. 1997). The also has direct on et al. 2000). It is that at one of is from infected cells and to cells et al. 2000). A and E viruses via the gut and may replicate however both rapidly to the and the features of both viruses are similar although is more severe and may have a rate of in has a incubation period than d vs 48 and a more prolonged et al. 1995; and 1997). The make identification of the of infection as food will usually have been or of before illness by the is and a shed in the and in the into the The and of the and become is from the by the and Virus particles are shed into the and in the but in to the caused by gastroenteritis viruses there is only with activities and new viruses are to the immune 2–3 after infection and to immune attack on infected It is this than the virus itself that causes the signs of the immune all infected cells thus the from the body. may be prolonged and some of cases may follow a over 12 months or viruses A and E have been affected by human In former infection occurred in often whilst protected by infections to be or viruses are rare is This has exposure and the age at which first infection in 30% of those under were seropositive in by this had to only although in the elderly In in has been for many of persons over have no antibody to have been This in age at infection increases the of below 3 infection is always but symptomatic infections by 5 years and with age et al. over years of age account for only 12% of the cases of but have a rate higher than 1994; 2004). This in infection a pool of individuals to in the community and conditions for Analysis of incidence in the US of 2004). The for 000 cases occurred on per year between and most were or free but 000 cases were et al. that 5% of cases are The in the UK has been et al. 2001). The of adults in some of the world is significant in the of food-borne infection trade that could food in of high to of low could a for adults in those (see E virus is not significant in the UK or most infections are limited to of are
M.J. Carter (Mon,) studied this question.