Non-O157 Shiga Toxin-Producing E. coli can cause food poisoning.
Escherichia coli (E. coli) bacteria are classified by their O and H antigens (e.g., E. coli O157:H7, E. coli O26:H11) and broadly categorized as Shiga toxin-producing E. coli (STEC) O157 or non-O157 STEC.
For many years, most recognized STEC outbreaks were associated with STEC O157. Despite the dominance of STEC O157, at least 150 non-O157 strains of E. coli are known to cause human illness and have been associated with outbreaks.
In the US, documented outbreaks of non-O157 E. coli include 10 involving O111; 6 involving O26; 3 involving O45; 2 involving O145, O104, and O6; and, one each involving O51; O103; O27; and, O84. Non-O157 STEC outbreaks are rare, but tend to primarily be due to contaminated food and person-to-person transmission.
Non-O157 STEC infections are under-recognized and under-reported due to inadequate epidemiological and laboratory surveillance. In the United States, E. coli O157:H7 became nationally notifiable in 1994, whereas non-O157 STEC infections were not reportable until 2000.  Screening for non-O157 STEC remains rare. This is no surprise since by 2007 only 66% of clinical labs screened all stool samples for E. coli O157:H7 and fewer than 10% of labs ever conducted on-site testing for non-O157 STEC. As with E. coli O157:H7, non-O157 STEC cases tend to occur during the summer months.
Non-O157 STEC can be difficult to identify in laboratory screening for E. coli O157 because they do not ferment sorbitol. Most stool cultures suspected to contain STEC are first screened for Shiga toxin; a positive test could be either E. coli O157:H7 or non-O157 STEC. Unfortunately, some labs will discard Shiga toxin-positive cultures after reporting to the referring doctor without identifying the strain. State laboratories can send STEC cultures to the CDC to determine the serotype. Some states, such as Minnesota and Connecticut have begun studies of their own to identify non-O157 STEC.
In recent years, improved diagnostic assays for non-O157 STEC have contributed to an increased appreciation of the severity of disease caused by these strains, including hemolytic uremic syndrome (HUS). Notably, the number of non-O157 STEC cases reported to CDC’s FoodNet has risen steadily each year; from 2000-2006, there was an overall 4-fold increase in incidence (0.12 cases per 100,000 to 0.42 cases per 100,000 population) at FoodNet sites. The most common serogroups reported to cause foodborne illness in the United States are O26, O111, O103, O121, O45, and O145.  These six serotypes account for 75% of human infections.
Outbreaks Caused By Non-O157 Shiga Toxin-Producing E. coli
Worldwide, non-O157 STEC outbreaks emerged in the 1980s, and the first reported outbreaks in the United States occurred in the 1990s. [57, 55] The number of reported outbreaks due to non-O157 STEC remains relatively low in the United States, but experts agree that documented outbreaks probably represent the “tip of the iceberg.” From 1983-2002, seven non-O157 STEC outbreaks were reported in the United States.  During the following five-year period from 2003-2007, CDC documented an additional five non-O157 STEC outbreaks (CDC Outbreak Surveillance Data).
An extraordinary non-O157 outbreak occurred in Germany beginning in May 2011. The STEC involved was extremely rare: E. coli O104:H4. It was also extremely virulent. Ultimately, the outbreak sickened nearly 4,000 people and killed more than 50. This strain was not only resistant to many antibiotics, it possessed a novel mechanism for sticking to intestinal cells. Other unusual aspects of this outbreak were that it affected a disproportionately large percentage of women. Further, nearly a quarter of those infected developed HUS and of those the vast majority was women. It appears that this non-O157 STEC acquired its particular virulence factors and antibiotic resistance through horizontal gene acquisition rather than point mutations or descent from prior generations of bacteria.  The outbreak was ultimately traced to contaminated seeds of fenugreek from Egypt, sold as sprouts by an organic farm in Germany.
A study of non-O157 STEC concluded that these strains may account for up to 20 to 50% of all STEC infections in the United States.  The prevalence of non-O157 STEC infections is placing an increasing burden on society and the health care system in the United States.