Sequelae of Foodborne Illness Caused by 5 Pathogens, Australia, Circa 2010 - Volume 20, Number 11—November 2014 - Emerging Infectious Disease journal - CDC
Volume 20, Number 11—November 2014
Research
Sequelae of Foodborne Illness Caused by 5 Pathogens, Australia, Circa 2010
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Abstract
In Australia circa 2010, 4.1 million (90% credible interval [CrI] 2.3–6.4 million) episodes of foodborne gastroenteritis occurred, many of which might have resulted in sequelae. We estimated the number of illnesses, hospitalizations, and deaths from Guillain-Barré syndrome, hemolytic uremic syndrome, irritable bowel syndrome, and reactive arthritis that were associated with contaminated food in Australia. Data from published studies, hospital records, and mortality reports were combined with multipliers to adjust for different transmission routes. We used Monte Carlo simulation to estimate median estimates and 90% CrIs. In Australia, circa 2010, we estimated that 35,840 (90% CrI 25,000–54,000) illnesses, 1,080 (90% CrI 700–1,600) hospitalizations, and 10 (90% CrI 5–14) deaths occurred from foodborne gastroenteritis–associated sequelae. Campylobacter spp. infection was responsible for 80% of incident cases. Reducing the incidence of campylobacteriosis and other foodborne diseases would minimize the health effects of sequelae.
Foodborne gastroenteritis is a major source of illness in Australia, causing an estimated 4.1 million (90% credible interval [CrI] 2.3–6.4 million) illnesses, 30,600 (90% CrI 28,000–34,000) hospitalizations, and 60 (90% CrI 53–63) deaths each year (1). In addition to the direct effects of these illnesses, infection with some pathogens can result in sequelae, which can be severe, require multiple hospitalizations, and be costly to society (2). We report on the effects of sequelae associated with Guillain-Barré syndrome (GBS), hemolytic uremic syndrome (HUS), irritable bowel syndrome (IBS), and reactive arthritis (ReA) from 5 pathogens acquired from contaminated food in Australia.
Each of these 4 sequel illnesses are preceded by different gastrointestinal infections and have unique characteristics. GBS, a rare but serious autoimmune illness, affects the nervous system and causes acute flaccid paralysis. GBS can occur as a sequel to Campylobacter spp. infection 10 days–3 weeks after gastrointestinal illness (3,4). HUS is characterized by acute renal failure, hemolytic anemia, and thrombocytopenia and can result from infection with Shiga toxin–producing Escherichia coli (STEC) ≈4–10 days after onset of gastroenteritis (5,6). IBS is a gastrointestinal disorder that causes abdominal pain and bowel dysfunction. It is not life threatening, but it can cause substantial health effects after illness with Campylobacter spp., nontyphoidal Salmonella entericaserotypes (hereafter referred to as nontyphoidal Salmonella spp.), or Shigella spp. (7,8). ReA is a type of spondyloarthritis that can develop up to 4 weeks after an enteric infection from Campylobacter spp., nontyphoidal Salmonella spp., Shigella spp., or Yersinia enterocolitica (9). We estimated the number of illnesses, hospitalizations, and deaths resulting from GBS, HUS, IBS, and ReA from selected foodborne pathogens in Australia in a typical year circa 2010.
We estimated the effects of foodborne sequelae acquired in Australia circa 2010 using data from multiple sources in Australia and from international peer-reviewed literature. We defined foodborne sequelae as illnesses occurring after bacterial gastroenteritis caused by eating contaminated food. Sequelae were defined as the secondary adverse health outcomes resulting from a previous infection by a microbial pathogen and clearly distinguishable from the initial health event (10). Illness can be acute, such as with HUS, or chronic (lasting for many years), as with IBS. We estimated incidence, hospitalizations, and deaths with uncertainty bounds using Monte Carlo simulation in @Risk version 6 (http://www.palisade.com/), which incorporates uncertainty in both data and inputs. Each stage of our calculation was represented by a probability distribution, and our final estimates of incidence, hospitalizations, and deaths were summarized by the median and 90% CrI. Similar to a recent study in the United States (11), we used empirical distributions for source distributions, such as the number of hospitalizations or deaths, to avoid assumptions about the expected shape of these distributions. All other inputs were modeled by using the PERT (project evaluation and review technique) distribution, which enables the input of a minimum, maximum, and modal value, or 3 percentile points, such as a median value and 95% bounds. We used this distribution widely in our analyses because it enables asymmetric distributions and can be produced from many data sources, including expert elicitation data. The Australian National University Human Research Ethics Committee approved the study.
Ms Ford is a research assistant in the infectious disease and modelling group at the National Centre for Epidemiology and Population Health at the Australian National University. Her research interests include infectious diseases.
Acknowledgments
We thank John Bates, Kathryn Brown, Duncan Craig, Margaret Curran, Patricia Desmarchelier, Gerard Fitszimmons, Katie Fullerton, Joy Gregory, David Jordan, Tony Merritt, Jennie Musto, Nevada Pingault, Jane Raupach, Craig Shadbolt, Martha Sinclair, Lisa Szabo, Hassan Vally, and Mark Veitch for their assistance with this study. We also thank the OzFoodNet network, public health laboratories, and health department staff in Australia for the robust collection of data on foodborne diseases.
This project was funded by the Australian Government Department of Health and Ageing, Food Standards Australia New Zealand and New South Wales Food Authority.
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Suggested citation for this article: Ford L, Kirk M, Glass K, Hall G. Sequelae of foodborne illness caused by 5 pathogens, Australia, circa 2010. Emerg Infect Dis [Internet]. 2014 Nov [date cited]. http://dx.doi.org/10.3201/eid2011.131316
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