Foodborne Illness Acquired in the United States—Major Pathogens

Scallan, Elaine; Hoekstra, Robert M.; Angulo, Frederick J.; Tauxe, Robert V.; Widdowson, Marc‐Alain; Roy, Sharon L.; Jones, Jeffery L.; Griffin, Patricia M.

doi:10.3201/eid1701.09-1101p1

Cited by 1,144 publications

(1,393 citation statements)

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“…Campylobacter jejuni and Salmonella are currently ranked the most important bacterial foodborne pathogens in the USA (Scallan et al, 2011). C. jejuni inhabits the gastrointestinal (GI) tract of poultry, cattle, sheep and swine (Blaser, 1997), and is most frequently transmitted to humans through carcass contamination that occurs during slaughter of meat animals (Jonsson et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

“…Poultry is the most important reservoir for human disease (Zhao et al, 2010;reviewed by Wassenaar, 2011). C. jejuni infection reportedly results in 850 000 cases of gastroenteritis and 76 deaths per year, which cost approximately $1.7 billion in the USA (Batz et al, 2011;Scallan et al, 2011;Snelling et al, 2005;Young et al, 2007). C. jejuni most frequently causes self-limiting gastroenteritis that does not require treatment.…”

Section: Introductionmentioning

confidence: 99%

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Passage of Campylobacter jejuni through the chicken reservoir or mice promotes phase variation in contingency genes Cj0045 and Cj0170 that strongly associates with colonization and disease in a mouse model

et al. 2012

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Human illness due to Camplyobacter jejuni infection is closely associated with consumption of poultry products. We previously demonstrated a 50 % shift in allele frequency (phase variation) in contingency gene Cj1139 (wlaN) during passage of C. jejuni NCTC11168 populations through Ross 308 broiler chickens. We hypothesized that phase variation in contingency genes during chicken passage could promote subsequent colonization and disease in humans. To test this hypothesis, we passaged C. jejuni strains NCTC11168, 33292, 81-176, KanR4 and CamR2 through broiler chickens and analysed the ability of passaged and non-passaged populations to colonize C57BL6 IL-10-deficient mice, our model for human colonization and disease. We utilized fragment analysis and nucleotide sequence analysis to measure phase variation in contingency genes. Passage through the chicken reservoir promoted phase variation in five specific contingency genes, and these 'successful' populations colonized mice. When phase variation did not occur in these same five contingency genes during chicken passage, these 'unsuccessful' populations failed to colonize mice. Phase variation during chicken passage generated small insertions or deletions (indels) in the homopolymeric tract (HT) in contingency genes. Singlecolony isolates of C. jejuni strain KanR4 carrying an allele of contingency gene Cj0170 with a 3These authors contributed equally to this work. Two supplementary tables, listing PCR primer sequences for fragment and sequence analysis used in this study, and results of sequence and fragment analysis to confirm large shifts in allele frequency, with a supplementary reference, are available with the online version of this paper. 10G HT colonized mice at high frequency and caused disease symptoms, whereas single-colony isolates carrying the 9G allele failed to colonize mice. Supporting results were observed for the successful 9G allele of Cj0045 in strain 33292. These data suggest that phase variation in Cj0170 and Cj0045 is strongly associated with mouse colonization and disease, and that the chicken reservoir can play an active role in natural selection, phase variation and disease.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Passage of Campylobacter jejuni through the chicken reservoir or mice promotes phase variation in contingency genes Cj0045 and Cj0170 that strongly associates with colonization and disease in a mouse model

et al. 2012

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“…In the United States, certain risk groups have been associated with deaths due to diarrhea and are more likely to be tested (3)(4)(5). Rapid and accurate detection of gastrointestinal (GI) pathogens is vitally important so that appropriate therapy can be initiated and proper infection control and epidemiologic measures can be taken to help curb the spread of disease (6)(7)(8).…”

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confidence: 99%

Comparative Evaluation of Two Commercial Multiplex Panels for Detection of Gastrointestinal Pathogens by Use of Clinical Stool Specimens

et al. 2014

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The detection of pathogens associated with gastrointestinal disease may be important in certain patient populations, such as immunocompromised hosts, the critically ill, or individuals with prolonged disease that is refractory to treatment. In this study, we evaluated two commercially available multiplex panels (the FilmArray gastrointestinal [GI] panel [BioFire Diagnostics, Salt Lake City, UT] and the Luminex xTag gastrointestinal pathogen panel [GPP] [Luminex Corporation, Toronto, Canada]) using Cary-Blair stool samples (n ‫؍‬ 500) submitted to our laboratory for routine GI testing (e.g., culture, antigen testing, microscopy, and individual real-time PCR). At the time of this study, the prototype (non-FDA-cleared) FilmArray GI panel targeted 23 pathogens (14 bacterial, 5 viral, and 4 parasitic), and testing of 200 l of Cary-Blair stool was recommended. In contrast, the Luminex GPP assay was FDA cleared for the detection of 11 pathogens (7 bacterial, 2 viral, and 2 parasitic), but had the capacity to identify 4 additional pathogens using a research-use-only protocol. Importantly, the Luminex assay was FDA cleared for 100 l raw stool; however, 100 l Cary-Blair stool was tested by the Luminex assay in this study. Among 230 prospectively collected samples, routine testing was positive for one or more GI pathogens in 19 (8.3%) samples, compared to 76 (33.0%) by the FilmArray and 69 (30.3%) by the Luminex assay. Clostridium difficile (12.6 to 13.9% prevalence) and norovirus genogroup I (GI)/GII (5.7 to 13.9% prevalence) were two of the pathogens most commonly detected by both assays among prospective samples. Sapovirus was also commonly detected (5.

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“…CPE-producing type A strains are responsible for nearly a million food poisoning (FP) cases annually in the United States (6,7). C. perfringens type A strains producing CPE also cause ϳ5 to 15% of all cases of human antibiotic-associated diarrhea (AAD) or sporadic diarrhea (SD) (1,2,8).…”

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confidence: 99%

Contributions of NanI Sialidase to Caco-2 Cell Adherence by Clostridium perfringens Type A and C Strains Causing Human Intestinal Disease

McClane

2014

Infect Immun

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Previous studies showed that Clostridium perfringens type D animal disease strain CN3718 uses NanI sialidase for adhering to enterocyte-like Caco-2 cells. The current study analyzed whether NanI is similarly important when type A and C human intestinal disease strains attach to Caco-2 cells. A PCR survey determined that the nanI gene was absent from typical type A food poisoning (FP) strains carrying a chromosomal enterotoxin (CPE) gene or the genetically related type C Darmbrand (Db) strains. However, the nanI gene was present in type A strains from healthy humans, type A strains causing CPE-associated antibioticassociated diarrhea (AAD) or sporadic diarrhea (SD), and type C Pig-Bel strains. Consistent with NanI sialidase being the major C. perfringens sialidase when produced, FP and Db strains had little supernatant sialidase activity compared to other type A or C human intestinal strains. All type A and C human intestinal strains bound to Caco-2 cells, but NanI-producing strains had higher attachment levels. When produced, NanI can contribute to host cell attachment of human intestinal disease strains, since a nanI null mutant constructed in type A SD strain F4969 had lower Caco-2 cell adhesion than wild-type F4969 or a complemented strain. Further supporting a role for NanI in host cell attachment, sialidase inhibitors reduced F4969 adhesion to Caco-2 cells. Collectively, these results suggest that NanI may contribute to the intestinal attachment and colonization needed for the chronic diarrhea of CPE-associated AAD and SD, but this sialidase appears to be dispensable for the acute pathogenesis of type A FP or type C enteritis necroticans.

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Foodborne Illness Acquired in the United States—Major Pathogens

Cited by 1,144 publications

References 32 publications

Passage of Campylobacter jejuni through the chicken reservoir or mice promotes phase variation in contingency genes Cj0045 and Cj0170 that strongly associates with colonization and disease in a mouse model

Passage of Campylobacter jejuni through the chicken reservoir or mice promotes phase variation in contingency genes Cj0045 and Cj0170 that strongly associates with colonization and disease in a mouse model

Comparative Evaluation of Two Commercial Multiplex Panels for Detection of Gastrointestinal Pathogens by Use of Clinical Stool Specimens

Contributions of NanI Sialidase to Caco-2 Cell Adherence by Clostridium perfringens Type A and C Strains Causing Human Intestinal Disease

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