By Kelly A. Reynolds, MSPH, Ph.D.

On March 15, the infamous ’cruise ship virus‘ struck again. Reports of hundreds of ill passengers and crewmembers pervaded news reports. Concurrently, researchers in Toronto, Canada identified an association between norovirus outbreaks and source drinking water temperatures. Although the first identified norovirus (then called Norwalk virus) outbreak occurred in 1972, in Norwalk, CT, much is still being discovered about this elusive waterborne pathogen.

What are waterborne noroviruses?
Noroviruses are estimated to be the primary cause of food and waterborne outbreaks in the United States. Noroviruses are one of the most contagious stomach viruses that infect humans; cases number second only to the common cold. Human sera samples indicate that by the time we are 18 years old, more than 50 percent of us show evidence of exposure and immune response to norovirus. Reinfection is common and there is no lasting immunity to the pathogen.

Symptoms from norovirus are generally not life threatening although deaths do occur, particularly in elderly populations. Illness onset is usually within 24 to 48 hours and quite rapid, resulting in abdominal pain, malaise, low-grade fever, vomiting and nausea—common flu-like symptoms. Illness is generally self-limiting within 24 to 72 hours; thus, many victims do not seek medical treatment. For those who do, diagnostic tests are not likely to be ordered, and thus the majority of infections are not monitored or reported. Therefore, illness data on noroviruses are generally from outbreaks where cases are clustered and easier to identify; such as on cruise ships.

A member of the Caliciviridae family, they have been known by many names over the years, including: Norwalk viruses, Norwalk-like viruses, and small round structured viruses (SRSVs). The media has nicknamed norovirus infections as ‘the cruise ship virus‘, ‘gastric flu‘ and ’winter vomiting disease‘. Each of these nicknames reflects unique characteristics of the virus and its ability to sustain itself in the human population.

The cruise ship syndrome
The March 15 cruise ship outbreak affected 350 out of 1,829 passengers and continued after three consecutive trips from South Carolina. Three days prior, nearly 50 passengers fell ill on another cruise in Brazil. Interestingly, this was the first trip the ship had taken since it’s quarantine a week earlier following 310 cases of norovirus infection.

A trend with several cruise ship outbreaks showed that despite a thorough cleaning and sanitation protocol on the ship, the outbreak cycle was only broken after they were taken out of commission and more thoroughly sanitized. In one instance, items such as remote controls, bibles, poker chips and money were targeted for sanitizing and disinfecting. In addition, pillows were replaced and carpets steam-cleaned. Only after this collective effort was the cycle of the outbreak ended.

Cruise ships offer an opportunity to easily identify cases due to the closed quarters and captive population. Cruise ships have a stringent sanitation standard and are monitored and inspected under the Center for Disease Control’s Vessel Sanitation Program. (If you are planning a cruise soon, see http://www.cdc.gov/nceh/vsp/ for tips on staying healthy).

Winter vomiting disease
Another name for norovirus is the winter vomiting disease. Nearly all of the cruise ship outbreaks occurred in the winter months, and reports of additional cleaning efforts during the peak winter season of norovirus ’stomach flu‘ are anecdotally present on cruise line websites. While norovirus infections are known to increase in the winter, the reasons for their seasonality are not fully known. Recent research, however, supports the possibility that source water temperature plays an important role.

From November 2005 to March 2008, a group of Canadian researchers evaluated a total of 253 outbreaks of norovirus gastroenteritis.1 Local watershed conditions (temperature and flow) were found to be associated with outbreaks. This data supports the relative importance of drinking water reservoirs in norovirus transmission, and the role fluctuating source water conditions play in the seasonality of stomach infections. More research is needed, however, to prove whether or not the association between drinking water conditions and risk of norovirus infection are indeed causal.

In any case, the seasonal trend of norovirus infections consistently peaks in the winter, around October/November and begins to decline in March, but may persist through June. Multiple factors may affect the seasonality of norovirus infections. For example, do lower temperatures play a bigger role or decreased ultraviolet light in the winter?2 Understanding how long the viruses survive in the environment is an important component in the evaluation of associative public health risks.

Gastric flu
In 2007, the CDC published a summary of norovirus activity in the US, stating that there was a noted increase in cases.3 In addition, the number of outbreaks and fatalities due to noroviruses were on the rise in the nation. This was not an apparent increase in reporting but rather, a newly emerging condition involving the pathogen.

From October to December 2006, 24 states reported at least five norovirus outbreaks. Of these, 92 percent reported an increase over 2005 outbreak data, ranging from an increase of 18 to 800 percent. By 2007, the increase in norovirus incidence was linked to two new types of the organism, called GII.4 Minerva and GII.4 Laurens. These two types were responsible for 79 perccent of the outbreaks from 2006 to 2007.

Why these two strains behaved differently than other norovirus strains is not known. Scientists theorize that the emerging strains have the characteristic of being more virulent or more transmissible. Another theory is that the hosts (i.e., humans) have no immunity to the new strains and are more susceptible to infection.

Etiological agents of the flu (influenza virus) and the gastric flu (norovirus) share many characteristics.2 Like influenza, norovirus immunity does not effectively build in the community due the virus’ ability to sporadically change and become immunologically unrecognizable to the human immune system. Therefore, the predominantly circulating norovirus at any given season differs. Like influenza, development of a norovirus vaccine would require surveillance of the predominately circulating strains with manufacture and delivery of the appropriate vaccine strain.

Some individuals are genetically susceptible to norovirus infection.4 Persons who carry an FUT2 gene are more likely to be infected, but may also have a lesser ability to build post-infection immunity. Overall, norovirus immunity is short-lived and thus old and new strains of the virus can circulate together. On the other hand, in the case of influenza, longer-lasting immunity in a population is common and thus newer strains out-compete and replace older strains. In addition, unlike influenza, noroviruses do not have an animal host to aid in their circulation, but they will persist at lower levels in the summer and throughout the year.3

Conclusion
Inherent and newly discovered characteristics of noroviruses continue to provide insight into necessary controls needed. Despite more than three decades of attempts, a practical method for culturing noroviruses has not yet been established. The lack of a culture assay for the virus limits our understanding of its mutation, infectivity, and inactivation characteristics.

Research related to the persistence of noroviruses on surfaces and cruise ships has led to questions regarding drinking water treatment efficacy. Traditional drinking water treatments, such as chlorine disinfection, however, have been shown to inactivate noroviruses.5 Therefore, inadequate drinking water treatment or untreated groundwater sources are typically identified causes of waterborne norovirus outbreaks. Improved survival in cooler waters only increases the exposure risks.

POU treatment technologies such as nanofiltration, RO, distillation, and UV light are highly effective against noroviruses and, as with so many other waterborne pathogens, offer a final barrier to contaminants known to periodically flow through the tap.

References

  1. Greer, A.L., Drews, S.J., Fisman, D.N. 2010. Why ”winter” vomiting disease? Seasonality, hydrology, and norovirus epidemiology in Toronto, Canada. EcoHealth. Published online: February 12, 2010. Internation Association for Ecology and Health.
  2. Lopman, B, Zambon, M., Brown, D.W. 2008. “The evolution of norovirus, the “gastric flu”.” PLoS Medicine. 5:187-189.
  3. Centers for Disease Control and Prevention. 2007. Norovirus Activity—United States, 2006-2007, Morbidity and Mortality Weekly Report August 24, 2007; 56: 842-846.
  4. Lindesmith, L.C., Donaldson, E.F., LoBlue, A.D., et al., 2008. ”Mechanisms of GII.4 norovirus persistence in human populations.” PLoS Medicine. 5:269-290.
  5. Shin, G, Sobsey, M.D. 2008. “Inactivation of norovirus by chlorine disinfection of water.” Water Research. 42:4562-4568.

About the author
Dr. Kelly A. Reynolds is an Associate Professor at the University of Arizona College of Public Health. She holds a Master of Science Degree in public health (MSPH) from the University of South Florida and a doctorate in microbiology from the University of Arizona. Reynolds has been a member of the WC&P Technical Review Committee since 1997 She can be reached via email at reynolds@u.arizona.edu

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