Noroviruses: the perfect human pathogens?

Noroviruses are perhaps the perfect human pathogens. These viruses possess essentially all of the attributes of an ideal infectious agent: highly contagious, rapidly and prolifically shed, constantly evolving, evoking limited immunity, and only moderately virulent, allowing most of those infected to fully recover, therebymaintaining a large susceptible pool of hosts. These characteristics have enabled noroviruses to become the leading cause of endemic diarrheal disease across all age groups [1], the leading cause of foodborne disease [2], and the cause of half of all gastroenteritis outbreaks worldwide [3]. In the United States alone, noroviruses are responsible for an estimated 21 million cases of acute gastroenteritis annually, including >70 000 hospitalizations and nearly 800 deaths [2, 4, 5]. In developing countries, where the greatest burden of diarrheal disease occurs, noroviruses have been estimated to cause up to 200 000 deaths each year in children <5 years of age [6]. Although recognition of this immense disease burden is relatively recent, it is unclear whether it has long been present and failed to be recognized because of lack of sensitive diagnostics or if, in fact, noroviruses represent a truly emergent public health issue [7]. Regardless, attempts to address the overwhelming burden of norovirus disease first require an understanding of the complexity and efficiency with which these viruses spread. The success of noroviruses should come as no surprise once one considers how well adapted they are for transmission within human populations. First, noroviruses have an extremely low infectious dose (≥18 viral particles), coupled with copious viral shedding (10–10 viral copies per gram of feces), even among asymptomatic infections [8–10], suggesting that up to 5 billion infectious doses may be shed by an infected individual in each gram of feces. Second, noroviruses are environmentally stable, able to survive both freezing and heating (although not thorough cooking), are resistant to many common chemical disinfectants, and can persist on surfaces for up to 2 weeks [11].Third, there are a myriad of ways in which noroviruses may be spread, including direct contact between hosts via fecal-oral transmission, ingestion of contaminated foods or water, handling of contaminated fomites followed by hand-to-mouth contact, and—unique among enteric pathogens—via ingestion of aerosolized particles [12]. Finally, noroviruses are a genetically diverse group of virusesthatrapidlyevolve, leadingtoanapparent lack of prolonged cross-protective immunity following infection [13, 14]. Clearly, public health efforts to prevent and control the spread of noroviruses face an uphill battle. The investigation Repp and Keene [15] reported in this issue of the Journal provides a fascinating example of how a unique exposure and transmission scenario can result in a norovirus outbreak. In this outbreak, one member of a soccer team traveling to a tournament developed acute gastroenteritis, presumably because of an exposure prior to the trip. There was reportedly no opportunity for direct contact between this index case after her symptoms began and any of her teammates. Instead, some of the aforementioned characteristics that have made noroviruses so successful (eg, environmental stability, copious shedding in stool and vomit, aerosol spread) facilitated indirect spread of the virus. First, virus shed invomitus,andperhapsevenfeces,became aerosolized in a bathroomwhere the index casewas activelysymptomatic.Theseaerosolized particles then settled on a reusable shopping bag that contained lunch items to be consumed the following day. The authors note that neither the bag nor its contents were ever actually touched by the index case, who left to return home early the next morning before the lunch items were consumed. After handling the food items in this bag and consuming their contents, 7 of 11 individuals (64%) exposed in this manner became ill. Unfortunately, the authors were unable to differentiate between handling of the food packaging versus consumption of the foods they contained. Additionally, there Received and accepted 13 January 2012; electronically published 8 May 2012. Correspondence: Aron J. Hall, DVM, MSPH Division of Viral Diseases, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, 1600 Clifton Rd NE, Mailstop A-34, Atlanta, GA 30333 ([email protected]). The Journal of Infectious Diseases 2012;205:1622–4 Published by Oxford University Press on behalf of the Infectious Diseases Society of America 2012. DOI: 10.1093/infdis/jis251