About E. coli

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E. coli O157:H7

E. coli O157:H7 is a foodborne pathogen that causes food poisoning.

E. coli O157:H7 is one of thousands of serotypes of Escherichia coli. The testing done to distinguish E. coli O157:H7 from its other E. coli counterparts is called serotyping. [6] 

Pulsed-field gel electrophoresis (PFGE), sometimes also referred to as genetic fingerprinting, is used to compare E. coli O157:H7 isolates to determine if the strains are distinguishable. [3, 7] A technique called multilocus variable number of tandem repeats analysis (MLVA) is used to determine precise classification when it is difficult to differentiate between isolates with indistinguishable or very similar PFGE patterns. [8] 

E. coli O157:H7 was first recognized as a pathogen in 1982 during an investigation into an outbreak of hemorrhagic colitis associated with consumption of hamburgers from a fast food chain restaurant. [9]  Retrospective examination of more than three thousand E. coli cultures obtained between 1973 and 1982 found only one isolate with serotype O157:H7, and that was a case in 1975.[4, 9]  In the ten years that followed, there were approximately thirty outbreaks recorded in the United States. [10]  This number is likely misleading, however, because E. coli O157:H7 infections did not become a reportable disease in any state until 1987, when Washington became the first state to mandate its reporting to public health authorities. [11, 12]  Consequently, an outbreak would not be detected if it was not large enough to prompt investigation. [11, 13]

E. coli O157:H7’s ability to induce injury in humans is a result of its ability to produce numerous virulence factors, most notably Shiga toxin (Stx), which is one of the most potent toxins known to man. [4, 14, 15]  Shiga toxin has multiple variants (e.g., Stx1, Stx2, Stx2c), and acts like the plant toxin ricin by inhibiting protein synthesis in endothelial and other cells. [16]  Endothelial cells line the interior surface of blood vessels, and are known to be extremely sensitive to E. coli O157:H7, which is cytotoxigenic to these cells. [16]

In addition to Shiga toxin, E. coli O157:H7 produces numerous other putative virulence factors, including proteins which aid in the attachment and colonization of the bacteria in the intestinal wall and which can lyse red blood cells and liberate iron to help support E. coli metabolism. [17]

E. coli O157:H7 evolved from enteropathogenic E. coli serotype O55:H7, a cause of non-bloody diarrhea, through the sequential acquisition of phage-encoded Stx2, a large virulence plasmid, and additional chromosomal mutations. [18, 19] The rate of genetic mutation indicates that the common ancestor of current E. coli O157:H7 clades likely existed some 20,000 years ago. [20]  E. coli O157:H7 is a relentlessly evolving organism, constantly mutating and acquiring new characteristics, including virulence factors that make the emergence of more dangerous variants a constant threat. [21, 22] The prospect of emerging pathogens as a significant public health threat has been emphasized by the CDC for some time. [23] As Robert Tauxe of the CDC notes:

After 15 years of research, we know a great deal about infections with E. coli O157:H7, but we still do not know how best to treat the infection, nor how the cattle (the principal source of infection for humans) themselves become infected. [23]

Although foods of bovine origin are the most common cause of both outbreaks and sporadic cases of E. coli O157:H7 infections, outbreaks of illnesses have been linked to a wide variety of food items.  For example, produce has been the source of substantial numbers of outbreak-related E. coli O157:H7 infections since at least 1991. [13, 24]  Outbreaks have been linked to alfalfa, clover and radish sprouts, lettuce, and spinach. [31, 32]Other vehicles for outbreaks include unpasteurized juices, yogurt, dried salami, mayonnaise, raw milk, game meats, hazelnuts, and raw cookie dough. [10, 13, 30]

 

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