Abstract
Shiga toxin-producing Escherichia coli (STEC) cause illnesses ranging from mild diarrhea to ischemic colitis and hemolytic uremic syndrome (HUS); serogroup O157 is the most common cause. We describe the epidemiology and transmission routes for U.S. STEC outbreaks during 2010–2017. Health departments reported 466 STEC outbreaks affecting 4769 persons; 459 outbreaks had a serogroup identified (330 O157, 124 non-O157, 5 both). Among these, 361 (77%) had a known transmission route: 200 foodborne (44% of O157 outbreaks, 41% of non-O157 outbreaks), 87 person-to-person (16%, 24%), 49 animal contact (11%, 9%), 20 water (4%, 5%), and 5 environmental contamination (2%, 0%). The most common food category implicated was vegetable row crops. The distribution of O157 and non-O157 outbreaks varied by age, sex, and severity. A significantly higher percentage of STEC O157 than non-O157 outbreaks were transmitted by beef (p = 0.02). STEC O157 outbreaks also had significantly higher rates of hospitalization and HUS (p < 0.001).
Highlights
We describe the epidemiology of both O157 and non-O157 Shiga toxin-producing Escherichia coli (STEC) outbreaks
Among the 33 outbreaks associated with animal contact, an animal type was implicated in 65% (23) of O157 outbreaks and 82% (9) of non-O157 outbreaks, and a ruminant was an implicated animal type in all but one outbreak
STEC O157 outbreaks resulted in more severe illnesses
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. An estimated 265,000 Shiga toxin-producing Escherichia coli (STEC) infections occur in the United States annually, ranging in severity from mild diarrhea to ischemic colitis and hemolytic uremic syndrome (HUS). More than 100 STEC serogroups are associated with human illness; serogroup O157 is the most identified cause of STEC infection in the United States. Clinical laboratories have increasingly adopted culture-independent tests to detect Shiga toxin genes, resulting in increased detection of non-O157 STEC [4,5,6,7,8]. In 2010, the incidence of sporadic (not associated with an outbreak) non-O157 STEC infections detected through active sentinel surveillance surpassed STEC. Previous reports have described transmission modes and exposures for O157 and non-O157 STEC outbreaks separately, during different time frames [10,11]. From 2010–2017, STEC O157 outbreaks were reported approximately twice as often as non-O157 STEC outbreaks; the distribution of O157 and non-O157 outbreaks varied by age, sex, and severity whereas transmission mode exhibited little variation
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