The following points highlight four major diseases caused by foodborne viruses. The diseases are: 1. Polio 2. Hepatitis A and E 3. Gastroenteritis Viruses 4. Enteric Viruses.
Disease # 1. Polio:
The genus Enterovirus is made up of small (28 nm), single-stranded RNA viruses, and includes poliovirus, which was at one time the only virus known to be foodborne.
Polio can be a transient viraemia with an incubation period of 3-5 days and characterized by headache, fever and sore throat, but in a minority of cases it can progress to a second stage of persistent viraemia where the virus invades the central nervous system causing varying degrees of paralysis and even death.
like other enterovirus infections, poliovirus is more likely to produce an asymptomatic infection in very young children. From about the turn of the Century, however, improvements in hygiene and sanitation in industrialized countries meant that early infection and acquisition of immunity became less common.
As a result, the disease was widely feared as it became more frequent in older children and young adults where it was likely to be much more severe.
Polio is now virtually eradicated in developed countries due to the availability of very effective live and inactivated vaccines. At the time that mass-vaccination programmes were introduced in the 1950s, food was no longer important as a vehicle.
Previously, contaminated milk had been the principal source of foodborne polio but this route of infection had been controlled by improvements in hygiene. Polio does however remain endemic in many less developed countries where some cases may be foodborne.
Disease # 2. Hepatitis A and E:
A similar story applies to another enterovirus, Hepatitis A, the cause of infectious hepatitis. Improvements in public hygiene and sanitation in the developed world have reduced exposure to the virus so that, when it does occur, it tends to be later in life when the illness is more severe.
The incubation period varies between two and six weeks. During this period the virus multiplies in the cells of the gut epithelium before it is carried by the blood to the liver. In the later part of the incubation period the virus is shed in the faeces. Early symptoms are anorexia, fever, malaise, nausea and vomiting, followed after a few days by symptoms of liver damage such as the passage of dark urine and jaundice.
Like other enteric viruses, hepatitis A is transmitted by the faecal-oral route. Primarily it is spread by person-to-person contact but food- and waterborne outbreaks do occur. Milk, fruits such as strawberries and raspberries, salad vegetables such as lettuce, and shellfish are common food vehicles.
With the exception of those caused by shellfish, common source outbreaks are usually due to contamination by an infected food handler. The long incubation period of the illness often makes identification of the source extremely difficult.
For the same reason, it is difficult to say with any accuracy what proportion of hepatitis A cases are transmitted by food, although it has been estimated that about 3% of cases in the United States are food- or waterborne.
The agent of enterically transmitted non-A, non-B hepatitis has now been designated hepatitis E virus and molecular biology studies indicate it is a calici-like virus. It too is transmitted by the faecal-oral route and. produces illness after an incubation period of 40 days.
Disease # 3. Gastroenteritis Viruses:
A number of different viruses have been implicated in gastroenteritis by their presence in large numbers (up to 108-1010g-1) in diarrhoeal stools. In most cases it has not proved possible to culture the virus thus preventing their full characterization. As a result, classification has been based largely on morphology and geographical origin.
Although other, better characterized, viruses such as rotavirus, calicivirus and astrovirus are also known to cause diarrhoea, it is these less-well-defined agents that are responsible for most outbreaks of foodborne gastroenteritis where a virus is identified. In the United States they have been known as Norwalk-like agents after the virus which caused an outbreak of gastroenteritis in schoolchildren in Norwalk, Ohio in 1968.
In the UK, they are described as small round structured viruses (SRSVs) based on the fact that, when viewed in the electron microscope, they are particles about 25-30 nm in diameter possessing an amorphous structure lacking geometrical symmetry (Figure 8.22).
Recent research has shown that Norwalk virus is in fact a calicivirus and it seems likely that this may prove to be the case for other similar but serologically distinct SRSVs .
Foodborne viral gastroenteritis is characterized by an incubation period of 15-50 h followed by diarrhoea and vomiting which persists for 24-48 h. The infectious dose is not known.
Studies in model systems have suggested that doses as low as one cell culture infectious unit can produce infection but in polio vaccination an oral dose of 100 000 infectious units is given to ensure a success rate of at least 90%. The onset of symptoms such as projectile vomiting may be very sudden and unexpected and this can contribute to the further spread of illness.
Disease # 4. Enteric Viruses:
Enteric viruses may be introduced into foods either as primary contamination, at source where the food is produced, or as secondary contamination during handling, preparation and serving.
It is possible that salad vegetables fertilized with human excrement could be contaminated with viruses while in the field and although salads have been implicated in outbreaks, this could also have been the result of secondary contamination during preparation.
Evidence of unequivocal primary contamination is largely restricted to bivalve molluscan shellfish, such as clams, cockles, mussels and oysters, which have been implicated in numerous outbreaks of hepatitis and gastroenteritis.
In the UK between 1976 and 1987 there were several large outbreaks involving cockles from the Essex coast in which more than 2000 people were affected. Large outbreaks have also been reported from Australia and the United States, but these pale beside the outbreak of hepatitis A in Shanghai in 1988 when almost 300 000 were reported ill and contaminated cockles were identified as the source of infection.
The problem arises because these shellfish are grown in shallow, inshore, coastal waters that are often contaminated with sewage. Since they feed by filtering sea water to extract suspended organic matter, they also tend to concentrate bacteria and viruses from the surrounding environment.
Pumping rates can be quite substantial as an oyster will filter up to four litres of seawater per hour and concentrate micro-organisms in their gut by up to a thousand-fold.
It is possible to decontaminate shellfish by relaying them in clean waters (if these can be found) or removing them to special depuration plants where they are encouraged to filter water that is re-circulated and purified, usually by treatment with UV light or ozone. Depuration procedures have proved very successful for removing bacterial pathogens; coliform bacteria have been shown to be removed within 24-48 hours.
However the rate at which viruses are cleansed is much slower and less predictable. This is probably due to the small size of the virion compared with the bacterial cell and the relative strength of its attachment to the gut wall.
It has been suggested that virus particles ingested by the shellfish are taken up by macrophages and transported from the gut to tissues that are remote from the depuration process, though there is little evidence for this.
The problem is compounded by the fact that some shellfish, such as oysters, are consumed without any cooking and those that are cooked receive only a mild, relatively uncontrolled heat process in order to prevent the flesh assuming the consistency of rubber.
Studies on the heat inactivation of hepatitis A virus have led to the introduction of guidelines in the UK for the cooking of cockles which recommend that the internal temperature of the meat should reach 85-90 °C for 1.5 min. It is not known whether these guidelines provide an acceptable safety margin with regard to SRSVs since they cannot be cultured in vitro for their heat sensitivity to be determined.
Secondary contamination by infected food handlers is an alternative source of infection, particularly with those food items that are subject to extensive handling in their preparation and are consumed without reheating.
Usually the food handler is suffering from viral gastroenteritis at the time. One outbreak in the UK provides a graphic illustration of secondary contamination and also how the sudden onset of symptoms can catch victims unaware and exacerbate the problem.
The outbreak occurred at a hotel in the UK where over 140 people were ill. One chef vomited in the changing room lavatory and then immediately returned to food preparation. Later that day he had an episode of diarrhoea. Two days later another member of the kitchen staff vomited into a bin outside the kitchen door and the following day two staff vomited in the kitchen itself.
The epidemiological evidence strongly implicated the cold foods prepared by the chef who was found to be excreting the SRSV 48 h after his symptoms subsided. However it is clearly possible that several other foods may have been contaminated by droplets from the vomitus from other affected kitchen workers.
In 1982 a huge outbreak in the Twin Cities area of Minnesota was caused by a baker who was working during an episode of diarrhoeal illness. Despite claiming to have washed his hands thoroughly after a visit to the toilet, he transferred sufficient virus to the butter cream that he mixed by hand to cause an outbreak which affected at least 3000 people.
Shortly after in the same area, a second outbreak affecting 2000 people occurred in which a food handler contaminated salads during banquet catering.
There is no evidence yet of a persistent symptomless carrier state for these viruses. They are no longer apparent in patient’s stools shortly after recovery but this may simply reflect the insensitivity of electron microscopy as a detection method.
Control:
The problems of monitoring and control of foodborne viruses are very different to those posed by bacteria. Testing foods for the presence of pathogenic viruses is not possible since many cannot be cultured and the numbers present are too low to be detected by techniques such as electron microscopy.
An alternative would be to use more readily cultured viruses that are shed in the faeces, such as the vaccine polio strain, as indicator organisms for the presence of pathogenic enteric viruses.
However current extraction methods are very inefficient and the culture techniques, based on observation of a cytopathic effect in cell monolayers or plaques in cell monolayers under semi solid medium, are far more complex and expensive than bacteriological testing.
Already though, techniques based on immunoassay and nucleic acid probes with the polymerase chain reaction promise to improve both the sensitivity and speed of virus detection.
An interesting approach is to use coliphage, a bacteriophage which infects the enteric bacterium E. coli, as a viral indicator. Coliphages do not require expensive tissue culture techniques for their enumeration since they can be detected through their ability to form plaques in a lawn culture of a suitable strain of E. coli.
The problem of extraction of the coliphage from food remains however, and interpretation of the significance of their presence in foods is uncertain.
As with other problems of microbiological food safety, control of viral contamination is most effectively exercised at source. Primary contamination can be controlled by avoiding the fertilization of vulnerable crops with human sewage and the discharge of virus-containing effluents into shellfish-harvesting waters.
Secondary contamination is even harder to detect microbiologically and can only be controlled by the strict observance of good hygienic practices in the handling and preparation of foods. Prospects are poor for a vaccine against the gastroenteritis viruses since immunity following infection appears to be short lived.
Volunteers who were made ill by ingesting a faecal extract containing the Norwalk agent became ill again a year later when given the same extract a second time. A new vaccine against hepatitis A, based on normal hepatitis A virus inactivated with formaldehyde, was licensed for use in the UK in 1992.