Non-O157 shiga toxin-producing Escherichia coli (STEC) are the causative agents of zoonotic emerging infectious diseases, often of bovine origin. Below is a general review of non-O157 STEC prevalence studies in humans, cattle, and beef products.
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, following adoption of a position statement (2000 ID#1) by the Council for State and Territorial Epidemiologists (CSTE). At that time, the CSTE recognized that the threat to public health from STEC infections extended beyond just the E. coli O157:H7 serogroup.
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 (Brooks et al, 2005).
Johnson et al (2006) evaluated the emerging clinical importance of non-O157 STEC and concluded that these strains may account for up to 20 to 50% of all STEC infections in the United States. Clearly, the prevalence of non-O157 STEC infections is placing an enormous burden on society and the health care system in the United States.
Cattle as Reservoirs
Beef and dairy cattle are known reservoirs of E. coli O157:H7 and non-O157 STEC strains (Hussein, 2007; Hussein and Sakuma, 2005). In reviews of STEC occurrence in cattle worldwide, the prevalence of non-O157 STECs ranged from 4.6 to 55.9% in feedlot cattle, 4.7 to 44.8% in grazing cattle, and 0.4 to 74% in dairy cattle feces. The prevalence in beef cattle going to slaughter ranged from 2.1 to 70.1%. While most dairy cattle-associated foodborne disease outbreaks are linked to milk products, dairy cattle still represent a potential source of contamination of beef products when they are sent to slaughter at the end of their useful production life (termed “cull” or “spent” dairy cows); this “dairy beef” is often ground and sold as hamburger.
The high prevalence of non-O157 STEC in some cattle populations, combined with the lack of effective on-farm control strategies to reduce carriage, represents a significant risk of contamination of the food supply and the environment.
Numerous non-O157 STEC serotypes known to cause human illness are from bovine origin, thus putting the beef supply at-risk. Both E. coli O157:H7 and non-O157 STEC may colonize the gastrointestinal tract of cattle, and potentially contaminate beef carcasses during processing. Although not as well studied, the risk factors for contamination of beef products from cattle colonized with non-O157 STECs are probably the same or very similar to E. coli O157:H7. For example, cattle hides contaminated with E. coli O157:H7 during slaughter and processing are a known risk factor for subsequent E. coli O157:H7 contamination of beef products. One study showed that the prevalence of non-O157 STEC (56.6%) on hides is nearly as high as that found for E. coli O157:H7 (60.6%) (Barkocy-Gallagher et al, 2003).
Hussein and Bollinger (2005) evaluated published reports from over three decades and found that non-O157 STEC were more prevalent in beef products compared with E. coli O157. In their study, the prevalence of non-O157 STEC ranged from 1.7 to 58% in packing plants, from 3 to 62.5% in supermarkets, and an average of 3% in fast food restaurants. In a recent survey of retail ground beef products in the United States, 23 (1.9%) of 1,216 samples were contaminated with non-O157 STEC (Samadpour et al, 2009). In another study, researchers found a 10 to 30% prevalence of non-O157 STEC in imported and domestic boneless beef trim used for ground beef (Bosilevac et al, 2007).
Non-E. coli O157:H7 Outbreaks
Worldwide, non-O157 STEC outbreaks emerged in the 1980’s, and the first reported outbreaks in the United States occurred in the 1990’s (Hussein 2007; Brooks et al, 2005). The number of reported outbreaks due to non-O157 STECs 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 (Brooks et al, 2005). During the following five-year period from 2003-2007, CDC documented an additional five non-O157 STEC outbreaks (CDC Outbreak Surveillance Data, http://www.cdc.gov/foodborneoutbreaks/outbreak_data.htm).
Products Implicated in Previous Outbreaks
There is a paucity of information on the vehicles of transmission for human non-O157 STEC infections, but contaminated raw dairy products, produce, and water have been implicated in the United States (Brooks et al, 2005). A review of non-O157 STEC in Connecticut showed that exposures, including ground beef, were similar in both non-O157 STEC and E. coli O157:H7 cases, suggesting that the routes of transmission are similar (CDC 2007). Considering the relatively high prevalence of both E. coli O157:H7 and non-O157 STEC in cattle populations and their products, it is not surprising that ground beef and other beef products could be a common food vehicle.
Non-O157 STEC outbreaks attributed to ground beef and its sausage products have been documented outside the United States including Argentina, Australia, Germany, and Italy. These beef-related outbreaks involved 8 STEC serogroups (O1, O2, O15, O25, O75, O86, O111, and O160). HUS cases were reported in five of the six outbreaks, mostly striking children and the elderly.
More rigorous investigation into the cause of non-O157 STEC outbreaks is needed to better understand the role of beef products and other foods in the contamination of the human food supply with these strains. Bettelheim (2007) described non-O157 STECs as “under-rated pathogens.” Indeed, the surveillance trends suggest that if left unchecked, it is only a matter of time before the United States experiences large non-O157-related outbreaks. Amending FMIA regulations to include pathogenic non-O157 STEC strains under the definition of “adulterated” is an urgently needed step in the prevention and control of these potentially deadly pathogens.
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Bettelheim, K. A. 2007. The non-O157 shiga-toxigenic (verocytotoxigenic) Escherichia coli: under-rated pathogens. Crit Rev Microbiol. 33:67-97.
Bosilevac J. M., M. N. Guerini, D. M. Brichta-Harhay, T. M. Arthur, and M. Koohmaraie. 2007. Microbiological characterization of imported and domestic boneless beef trim used for ground beef. J Food Prot. 70:440-9.
Brooks, J. T., E. G. Sowers, J. G. Wells, K. D. Greene, P. M. Griffin, R. M. Hoekstra, and N. A. Strockbine. 2005. Non-O157 shiga toxin-producing Escherichia coli infections in the United States, 1983-2002. J Infect Dis. 192:1422-9.
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CDC. 2008. Shiga toxin-producing Escherichia coli: burden and trends. FoodNet News, Winter 2008. Available at: http://www.cdc.gov/FoodNet/news/2008/January_FoodNet_News.pdf
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Hussein, H. S. 2007. Prevalence and pathogenicity of shiga toxin-producing Escherichia coli in beef cattle and their products. J Anim Sci. 85:E63-72.
Hussein, H. S. and T. Sakuma. 2005. Prevalence of shiga toxin-producing Escherichia coli in dairy cattle and their products. J Dairy Sci. 88:450-65.
Johnson, K. E., C. M. Thorpe, and C. L. Sears. 2006. The emerging clinical importance of non-O157 shiga toxin-producing Escherichia coli. Clin Infect Dis. 43:1587-95.
Samadpour, M., V. Beskhlebnaya, and W. Marler. 2009. Prevalence of non-O157 enterohaemmorrhagic Escherichia coli in retail ground beef in the United States. 7th International Symposium on Shiga Toxin (Verocytoxin)-producing Escherichia coli Infections. Buenos Aires, Argentina.