Water Conditioning & Purification Magazine

Patterns of Persistence in Waterborne Winter Vomiting Disease

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

In the late 1920s, Dr. J. Zahorsky coined the term ‘winter vomiting disease’ to describe sudden onset—but generally self-limiting—nausea and vomiting, primarily occurring in patients between September and March.1 Symptoms generally included diarrhea, headache and mild fever as well. At the time of Zahorsky’s diagnosis, little was known about the causative agent, now identified as noroviruses. More than 80 years later, norovirus remains a leading cause of food and waterborne illness around the world. Recent studies continue to provide new insights as to why this virus is so persistent in the human population.

Historical norovirus outbreaks
Since being documented in the 1920s, outbreaks of winter vomiting disease continued in epidemic proportions into the 1930s. A flurry of research articles was published in the literature throughout the 1950s on the topic of the mostly mild, but widespread syndrome. Certain patterns emerged relative to the epidemiology of the winter outbreaks. In particular, they had the novel characteristic of occurring in crowded school, hotel, cruise ship, military or camp settings. Today, outbreaks continue to be documented in nursing homes, retirement communities, hospitals and daycare centers. The winter vomiting disease was given a new name in 1968 following a series of outbreaks investigated by the National Communicable Disease Center, in cooperation with various health departments in the state of Ohio. One such outbreak started in late October of that year where nausea, vomiting and stomach cramps afflicted 50 percent of the student and teacher population at a local elementary school. The town was Norwalk, Ohio; hence, the term Norwalk virus would eventually be used to describe the etiological agent of the outbreak. Food was eliminated as a vehicle of disease transmission given that individuals who packed their lunch had the same odds of getting sick as those who didn’t. Water, however, could not be eliminated, as the school’s private well presented no chlorine residuals. Water remains one of the primary transmission routes of norovirus infection.

Additional information from the Ohio outbreak characterized the contagious nature of the agent. Family contacts with sickened primary cases resulted in a secondary attack rate of 32 percent, where barely 48 hours following illness in the primary population, other members of the household also became ill. Determining the cause of the Norwalk outbreak was difficult. Methods were not available for detecting this novel viral pathogen. Identification of the causative agent, therefore, became a matter of eliminating other possible etiologies. After ruling out common culturable bacteria, such as Salmonella, Shigella, E. coli and Staphylococcus aureus, a virus was suspected. Later, Norwalk-like virus structures visualized via microscopy would be termed simply as small round structured viruses or SRSVs.

Today, human caliciviruses are still referred to by multiple names, including: Norwalk virus, noroviruses or the common misnomer of stomach flu (the flu is a respiratory infection specifically caused by influenza viruses). The general public will also categorize norovirus symptomology as a general food poisoning without notice of the multiple transmission routes possible, including water or secondary spread from person-to-person, or person-to-surface-to-person contacts.

After the invention of molecular methods for definitive genetic identification and classification of biological organisms, members of the genus Norovirus were classified under the family of Caliciviridae, circa 2002. These detection tools were utilized to prove that noroviruses were a complex and moving target for infection control strategies.

Patterns of disease transmission
Today, norovirus is responsible for 96 percent of all viral gastroenteritis in the world, resulting in over 267 million infections per year. It is also thought to cause 50 percent of all food and waterborne outbreaks, or 23 million infections in the US.2 Norovirus disease in the US results in over 50,000 hospitalizations and 310 fatalities each year.3 Most infections are self limiting (within 24 to 72 hours) but for some (in particular the young and elderly), infections can be serious or fatal. One of the most defining characteristics of norovirus infection is the sudden onset of symptoms. Individuals tend to feel completely healthy but become rapidly nauseous, which proceeds quickly to sudden vomiting (commonly projectile) before one has the opportunity to retreat. Thus, stories of norovirus outbreaks among swimmers, football players and restaurant patrons are common. In other words, people are going about their daily activities when illness strikes. This, of course, gives norovirus a competitive advantage for transmission relative to other infectious agents that have you feeling the early effects of illness to where you prefer to stay at home.

Another characteristic of the notorious norovirus is that they have a very low infectious dose. Ingestion or inhalation of fewer than 10 viral particles is enough to transmit disease to an individual, whereas someone with norovirus infection can shed millions of viruses into the environment. Shedding may continue for up to three weeks post initial infection, providing additional opportunity for virus spread. Once in the environment, noroviruses are very difficult to eliminate. They can withstand freezing, heating to 60°C (140°F), alcohol sanitizers and other common practices of disinfection.2 While chlorine is an effective norovirus disinfectant, a full 10-minute contact time is recommended to eliminate the pathogen from contaminated surfaces. Not following this recommended protocol is partly the reason for the persistent pattern of norovirus transmission recently documented on cruise ships.4

Future predictions
The importance of the norovirus genome became apparent after the viral RNA was sequenced in 1990.5 Similar to the influenza virus, there are many genetic variants within the norovirus family. Minimally, there are 40 different strains divided into five groups based on genetic similarity (i.e., genogroups). Interestingly, strain 4 in genogroup 2 (GII.4) causes more than 80 percent of all norovirus infections around the world and thus, the majority of pandemic spread of the disease. Following infection, humans are typically immune to that particular norovirus variant for two to three years. Immunity to one strain of norovirus, however, does not confer immunity to other strains. While some genetically related norovirus strains circulating today were also known to circulate in the 1960s, the globally dominant GII.4 variant evolved sometime after 1980.2

Host immunity is a complicated, integrated series of defense mechanisms and susceptibilities that change over time and space. Recently, it was discovered that humans with blood type O were more susceptible to norovirus infection compared to those with other blood types. Conversely, the presence or absence of specific genes in some humans, coding for certain proteins or enzymes infers immunity to norovirus infections. In early feeding studies, these lucky individuals could not be infected with norovirus—they were simply resistant. Noroviruses, like influenza, frequently change their genetic structure and make-up, enabling them to outsmart the human immune response, which is largely based on recognition of previous pathogen exposures. Even persons genetically predisposed to resist norovirus infection of one strain appear to be susceptible to other genogroups. In other words, there is a norovirus strain for everyone!

The incidence of norovirus infections has not decreased. In fact, the highest number of norovirus outbreaks on record were documented for the winter of 2002-2003 in the US and Europe.2 Norovirus is also not just a wintertime disease; outbreaks can occur at all times of the year. At its most basic nucleic acid structure, these viruses have learned to overcome human defenses with efficient survival, low infectious dose, high shedding concentrations and rapidly changing genomes.

Half of all waterborne outbreaks in the US are likely due to norovirus. Endemic infections are common and typically not reported. Thus, experts theorize that norovirus infections are a much greater health burden than the outbreak surveillance data suggests. This same condition was noted in 1965 when authors wrote that many winter vomiting infections were not being reported and identified due to the rapid recovery rate from the illness.6

For reasons still unknown, norovirus clusters appear to be evolving more rapidly, producing a new group of infective strains every two to three years. Thus, with rapidly evolving strains of norovirus, epidemic and pandemic disease transmission is predicted to continue. Drinking water sources provide a plausible POU approach for minimizing norovirus exposures, and preventing norovirus transmission via water involves a multi-barrier approach. Being a fecal pathogen, sewage contamination of drinking water sources should be controlled. Appropriate chlorine residuals must be maintained. Reverse osmosis, distillation, ozone and UV light are also effective methods for reducing viral contamination in drinking water sources.


  1. 1. Zahorsky J. 1929. Hyperemesis hiemis or the winter vomiting disease. Archives in Pediatrics, 46: 391-395.
  2. Donaldson, E.F.; Lindesmith, L.C.; Lobue, A.C.; Baric, R.S. 2008. Norovirus pathogenesis: mechanisms of persistence and immune evasion in human populations. Immunological Reviews, 225: 190–211.
  3. Mead, P.S.; Slutsker, L.; Dietz, V.; McCaig, L.F. et al., 1999. Food-related illness and death in the United States. Emerging Infectious Diseases, 5: 607-625.
  4. CDC. Outbreak updates for international cruise ships. Vessel Sanitation Program. Updated July 26, 2011.
  5. Jiang, X.; Graham, D.; Wang, K.; Estes, M. 1990. Norovirus genome cloning and characterization. Science, 250: 1580-1583.
  6. Anonymous. Winter vomiting disease. British Medical Journal, 5468: 953-954.

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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