Ahead of Print -Geographic Divergence of Bovine and Human Shiga Toxin–Producing Escherichia coli O157:H7 Genotypes, New Zealand - Volume 20, Number 12—December 2014 - Emerging Infectious Disease journal - CDC
Volume 20, Number 12—December 2014
Geographic Divergence of Bovine and Human Shiga Toxin–Producing Escherichia coliO157:H7 Genotypes, New Zealand
Shiga toxin–producing Escherichia coli (STEC) O157:H7 and related non-O157 STEC strains are zoonotic pathogens that can cause severe gastrointestinal illness in humans; clinical signs and symptoms of disease range from diarrhea and hemorrhagic colitis to life-threatening hemolytic uremic syndrome (1,2). Ruminants, asymptomatic carriers of STEC, shed the pathogen in their feces, and are considered a primary source of foodborne and environmental outbreaks of STEC infection in humans (3).
The incidence of STEC infections in New Zealand has been among the highest in the world. In 2012, a total of 147 clinical STEC cases (3.3 cases/100,000 population) were notified, of which 142 were confirmed (4). Consistent with observations in previous years, the predominant serotype among the confirmed cases was O157:H7 (83.8%; 119/142). STEC became a notifiable disease in New Zealand in 1997, and since then, the annual number of notifications has increased steadily (4). Although the spatial distribution of STEC cases in New Zealand suggests an association with farming and other rural activities, limited epidemiologic data are available on the transmission pathways of STEC from cattle to humans.
The objectives of this research were to 1) compare the population structure and geographic distribution of different genotypes of STEC O157:H7 isolates from bovine and human sources in New Zealand; 2) assess evidence for localized transmission of STEC from cattle to humans in New Zealand; and 3) compare the genotype distribution of isolates from New Zealand with those from Australia, the predominant historic source of imported New Zealand cattle (5), and the United States. To investigate the molecular divergence of isolates, we used 2 molecular typing methods: Shiga toxin–encoding bacteriophage insertion (SBI) typing and pulsed-field gel electrophoresis (PFGE) profiling. Although PFGE can provide an indication of genomic similarities, it cannot provide a reliable measure of genetic relatedness of isolates, and the visual assessment of bands on an agarose gel to create PFGE profiles can result in misclassification bias (6). By using 2 methods and by examining the concordance between them, we could use the combined genotyping datasets to assess structuring and patterns of diversity among STEC O157:H7 isolates of bovine and human origin in New Zealand.
Dr Jaros is a postdoctoral research fellow at the Molecular Epidemiology and Public Health Laboratory, Hopkirk Research Institute at Massey University. Her research interests include the molecular epidemiology of infectious diseases.
We thank Muriel Dufour, Brent Gilpin, Kari Gobius, and Glen Mellor for their contributions and Charlotte Bolwell for very helpful comments on this manuscript.
This work was supported by the Meat Industry Association of New Zealand and the Ministry for Primary Industries.
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Suggested citation for this article: Jaros P, Cookson AL, Campbell DM, Duncan GE, Prattley D, Carter P et al. Geographic divergence of bovine and human Shiga toxin–producing Escherichia coli O157:H7 genotypes, New Zealand. Emerg Infect Dis. 2014 Dec [date cited].http://dx.doi.org/10.3201/eid2012.140281
1Preliminary results from this study were presented at the New Zealand Veterinary Association Conference; June 16–20, 2014, Hamilton, New Zealand.