Human noroviruses (NoV) are now the most common cause of outbreaks of epidemic non-bacterial gastroenteritis world-wide.
Highly infectious, nightmare to control, 100 billion virus particles per gram of faeces.
Previously known as Norwalk-like viruses (NLVs) and small round structured viruses (SRSVs), these viruses belong to the Caliciviridae family and are 26-35 nm non-enveloped single stranded positive-strand RNA viruses. That’s really, really small.
Each virus is ~30nm wide. Visible light has wavelengths between 300-700nm. Eeek!
The noroviruses are probably the single most infectious agents known. Their low infectious dose (1-10 virions), resistance to most chemical agents, prolific faecal shedding in those infected (100×109 per gram of stool) – which can continue for two months after symptoms have ceased – all militate towards making this a right little bastard to keep on top of. If it gets into a food business it’s a nightmare to get rid of it.
Noroviruses are divided into 5 genogroups, GI-V, of which GI, GII and GIV are known to infect humans. Over 25 different human genotypes are now recognised. Since 2002, genotype GII.4 strains have been the most common cause of outbreaks. Recombinant NoV strains have also been identified. Norwalk virus, GI.1, is the prototype strain. Norovirus identification has been difficult prior to development of molecular methods because human noroviruses cannot be cultured, and their wide genetic diversity limits the use of traditional immunology and serotyping assays.
Growth and Control
Human norovirus has not been grown in vitro and there is still no suitable animal model. This makes it difficult to study. The murine norovirus strain is readily culturable but not ideal. NoV detection is carried out using conventional or – better – real time RT-PCR. This is accurate but seriously expensive and is only likely to be used to investigate a serious outbreak. The illness is self limiting and the clinical diagnosis is accurate enough. There is an ELISA test but it’s pretty crap.
It’s reasonably stable on surfaces but not hugely so; a week is a reasonable assumption as you need a rare confluence of circumstances for it to last longer.
High-level oxidsers or 10,000ppm chlorine. Standard disinfectants ineffective.
The virus retains infectivity after incubation at 60°C for 30 min pasteurisation is not sufficient to eliminate it and resistance is reported to be greater in foods and shellfish. Steaming of bivalve shellfish is unlikely to inactivate NoV – and any cooking process that will would render the shellfish pretty much inedible. 100°C for 5mins will do it.
Under refrigeration and freezing conditions the virus remains intact and viable for several years.
Resists gastric acids at pH 3-4. The virus retained infectivity after exposure to pH 2.7 for 3 hr at room temperature. Believed to be sensitive to pH >9.0 (but unproven cos you can’t really test) so the pH in commercial dish wash detergents will render it inactive.
Based on data for other enteric viruses and virus indicators, it is likely that NoV persist in waters for extended periods (possibly weeks/months). NoV has caused many waterborne outbreaks and are often detected in environmental waters.
Infectious NoV has been detected on environmental surfaces, including carpets, for up to 12 days after NoV outbreaks.
Unknown but likely to be resistant.
Dose-response studies shows that NoV is resistant to inactivation following treatment with free residual chlorine of 0.5 to 1.0 mg/ml – the level of free chlorine consistent with that generally present in a drinking water supply.
Incubation: 10-50 hours (mean 24h) following ingestion of the virus.
Symptoms: Vomiting, often projectile, is generally the predominant symptom and is present in > 50% of cases. Stomach cramps, watery non-bloody diarrhoea, abdominal pain, low-grade fever and headache are other common symptoms. The duration of illness is usually between 24-60 hr. Diagnostic criteria are often used in the absence of virological confirmation.
Excretion of the virus in stools occurs from onset for up to 8 weeks following infection, with peak excretion rate at 4 days. Noroviruses are frequently discharged in vomit. The disease is generally mild and self-limiting. Hospitalisation is not generally required, but has been reported in some outbreaks. Attack rates are high, generally around 40-60% and sometimes as high as 80%.
Condition: Gastroenteritis. Norovirus colonise the proximal region of the small intestine and cause development of mucosal lesions with broadening and shortening of the microvilli. Short-term maladsorption of fats and some sugars has been reported. Abnormal gastric motor function is believed to be the cause of associated nausea and vomiting. The exact mechanism of pathogenesis remains unclear. Susceptibility or resistance to certain strains of HuNoV appears to be associated with human histo-blood group antigens (HBGA) Immunity is generally short lived, and is not sufficiently cross-reactive to protect against different norovirus strains.
Dose: Infective dose is estimated at 1-10 particles. Consumption of 1 virus particle may cause infection in 50% of occasions in susceptible people.
At Risk Groups: Affects all age groups, but the elderly and the immuno-compromised are particularly susceptible.
Long Term Effects: There is no evidence of any long-term sequelae following norovirus infection. Fatalities, which mostly occur in elderly patients, are rare in the developed world.
Treatment: Usually none, but fluids may be given to reduce the risk of dehydration.
Reservoirs / Sources
Human: The only known direct source for human NoV is human faeces or aerosolised vomit. Other indirect sources are shellfish, contaminated foods, water, fomites and the environment.
Animal: Bovine, feline, ovine and porcine noroviruses have been identified but there are no reports of cross-species transmission to humans as yet. Overseas, human GII NoV sequences have been identified in swine. Other caliciviruses have been found in various animal species.
Food: Contaminated bivalve shellfish, fresh produce (eg. herbs, lettuce, salads), water, ice and manually prepared ready-to-eat foods (including bakery items). Poor hygiene practices by food harvesters, processors and food handlers are a significant source.
Environment: Faeces from infected humans may contaminate soil or water. Faecal pollution from sewage discharges, septic tank leachates and boat discharges has caused contamination of shellfish beds, recreational water, irrigation water and drinking water. NoV are believed to survive for long periods in the environment and have been detected in shellfish 8-10 weeks after contamination.
Transmission Routes: The faecal/oral route is the established route of transmission. Infection occurs following ingestion of faecally-contaminated food and water. Another important route is person-to-person spread via aerosolised vomit following projectile vomiting. Direct transmission via contaminated surfaces, especially carpets, is also now considered a significant route; These routes contribute to the explosive outbreaks that cannot be attributed to faecal/oral spread alone. They generally occur in semi-closed communities such as rest homes, cruise ships and camps where there is close quarter living and often there may be reduced hygiene levels. There is evidence that asymptomatic food handlers can also cause infection and may excrete high numbers of NoV in their faeces.
Plague and Pestilence
Because of the relatively high attack rate, large numbers of people are often infected and most cases of disease are outbreak-related. Most foodborne outbreaks are ascribed to cross contamination via a food handler or inadequate cooking of previously contaminated foods. However, any food that becomes contaminated can act as a vehicle. Uncooked or lightly cooked bivalve shellfish such as oysters and mussels present a risk to health if grown in faecally contaminated waters.