Norovirus Genotype Profiles Associated with Foodborne Transmission, 1999–2012 - Volume 21, Number 4—April 2015 - Emerging Infectious Disease journal - CDC

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Norovirus Genotype Profiles Associated with Foodborne Transmission, 1999–2012 - Volume 21, Number 4—April 2015 - Emerging Infectious Disease journal - CDC

Volume 21, Number 4—April 2015

Research

Norovirus Genotype Profiles Associated with Foodborne Transmission, 1999–2012

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• Methods
• Results
• Discussion
• Suggested Citation

Figures

• Figure 1
• Figure 2
• Figure 3

Tables

• Table

Technical Appendicies

• Technical Appendix

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Linda Verhoef1 , Joanne Hewitt1, Leslie Barclay1, Sharia Ahmed, Rob Lake, Aron J. Hall, Ben Lopman, Annelies Kroneman, Harry Vennema, Jan VinjA(c), and Marion P. Koopmans

Author affiliations: National Institute for Public Health and the Environment, Bilthoven, the Netherlands (L. Verhoef, A. Kroneman, H. Vennema, M. Koopmans); Institute of Environmental Science and Research, Porirua, New Zealand (J. Hewitt, R. Lake); Centers for Disease Control and Prevention, Atlanta, Georgia, USA (L. Barclay, S.M. Ahmed, A.J. Hall, B. Lopman, J. VinjA(c)); Erasmus Medical Center, Rotterdam, the Netherlands (M. Koopmans)

Suggested citation for this article

Abstract

Worldwide, noroviruses are a leading cause of gastroenteritis. They can be transmitted from person to person directly or indirectly through contaminated food, water, or environments. To estimate the proportion of foodborne infections caused by noroviruses on a global scale, we used norovirus transmission and genotyping information from multiple international outbreak surveillance systems (Noronet, CaliciNet, EpiSurv) and from a systematic review of peer-reviewed literature. The proportion of outbreaks caused by food was determined by genotype and/or genogroup. Analysis resulted in the following final global profiles: foodborne transmission is attributed to 10% (range 9%%–11%) of all genotype GII.4 outbreaks, 27% (25%–30%) of outbreaks caused by all other single genotypes, and 37% (24%%–52%) of outbreaks caused by mixtures of GII.4 and other noroviruses. When these profiles are applied to global outbreak surveillance data, results indicate that ≈14% of all norovirus outbreaks are attributed to food.

Noroviruses are a leading cause of gastroenteritis worldwide. They belong to the family Caliciviridae and consist of an ≈7.5-kb genome in 3 open reading frames (ORFs). The first ORF (ORF1) encodes a polypeptide; ORF2 encodes the viral capsid protein (VP1); and ORF3 encodes a minor structural protein (VP2). Noroviruses are classified into at least 6 genogroups, GI–GVI (1). According to a recent unified proposal for nomenclature, genogroups are further subdivided into at least 38 genetic clusters (genotypes) (2). Noroviruses are environmentally stable (3) and can be transmitted by different routes (e.g., foodborne, personborne, waterborne, and environmental). Determining the transmission route during an outbreak investigation is complicated because transmission can occur by multiple routes in a single outbreak. After primary introduction of the virus through food, secondary person-to-person and environmental transmission can rapidly take over, making it hard to trace the disease back to contaminated food. Another complexity is that foodborne transmission can follow different routes as well; food can be contaminated during production (4) or during handling by an infected food handler (5).

Different exposure attribution methods (i.e., epidemiologic investigations, microbiological typing/subtyping, intervention studies, and expert elicitations) have been used to estimate the foodborne proportion of the overall disease incidence caused by a pathogen. Each approach has its advantages and disadvantages, and therefore the use of multiple methods has been recommended (6). Information about pathogen strain or subtypes may be of value for attribution but is dependent on substantial amounts of contextual data. For example, a method commonly used to attribute Salmonella spp. infections to a specific source uses strain collections representative of the pathogen in each of these sources (7).

For noroviruses, genogroup-specific differences have been reported with regard to environmental persistence (8), sensitivity to removal (9), and binding to receptors (10). These biological differences may underpin strain-specific epidemiologic patterns, suggesting a potentially useful approach for norovirus attribution. Such an approach was recently developed in a norovirus attribution study, which showed that the proportion of foodborne and person-to-person outbreaks differed between genotypes; the GI genotypes were more likely to be foodborne, and the II.4 genotype was more likely to be personborne (11). These findings indicate that genotype profiles may help distinguish which outbreaks are more likely to be foodborne than personborne. Also, a recent study on norovirus outbreaks in the United States showed that GI.3, GI.6, GI.7, GII.3, GII.6, and GII.12 were the norovirus genotypes most often associated with foodborne outbreaks and that, of the outbreaks with a known transmission route, 16% were foodborne (12). Norovirus infections, however, are a global problem, and efforts are under way to estimate the global social and economic costs of foodborne norovirus illness (13,14). To estimate the proportion of outbreaks attributed to foodborne transmission from a global perspective, we used aggregated norovirus outbreak data and genotyping information from different outbreak surveillance systems and from peer-reviewed literature.

Dr. Verhoef is an epidemiologist in the Center of Infectious Disease Control of the National Institute for Public Health and the Environment. Her work focuses on the epidemiology and surveillance of infectious diseases, particularly on the use of molecular typing information to facilitate source tracing activities.

Acknowledgments

We thank the World Health Organization's Foodborne Disease Burden Epidemiology Reference Group for financial support and critical review of this study, and we thank the FBVE and Noronet networks for collecting and sharing sequences.

The New Zealand Ministry of Health funded the work conducted by the ESR. This study was commissioned and paid for in part by the Foodborne Disease Burden Epidemiology Reference Group of the World Health Organization, the New Zealand Ministry of Health, and by the Government of the Netherlands on behalf of the Foodborne Disease Burden Epidemiology Reference Group.

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Figures

• Figure 1. Norovirus data for which the genotyped region and transmission mode were reported in different surveillance systems (FBVE/Noronet, 5,583 outbreaks in 22 countries (1999–2012); CaliciNet, 3,094 outbreaks in 1 country...
• Figure 2. Countries from which norovirus outbreak reports were included in analyses of norovirus genotype profiles associated with foodborne transmission, according to Foodborne Viruses in Europe/Noronet (1999–2012), CaliciNet (2009–2012), ESR-EpiSurv (2008–2012),...
• Figure 3. Genotype profiles. Foodborne proportion per genotype group per year, as reported to Foodborne Viruses in Europe/Noronet, with polymerase genotypes (n = 4,580) or, if missing, capsid genotypes (n =...

Table

• Table. Proportion of foodborne outbreaks per category, estimated according to different databases for 2009–2012

Technical Appendix

• Technical Appendix.  107 KB

Suggested citation for this article: Verhoef L, Hewitt J, Barclay L, Ahmed S, Lake R, Hall AJ, et al. Norovirus genotype profiles associated with foodborne transmission, 1999–2012. Emerg Infect Dis. 2015 Apr [date cited]. http://dx.doi.org/10.3201/eid2104.141073

DOI: 10.3201/eid2104.141073

1These authors contributed equally to this article.