West Missouri Beef, LLC has voluntarily recalled 14,000 pounds of boneless beef products due to potential contamination by E. coli O157:H7.  USDA’s Food Safety and Inspection Service (FSIS) announced the Class I recall in a press release last night.  It is the third Class I recall this year, and the fifth since November, adding up to 1,636,000 pounds of beef products that have been recalled due to potential E. coli O157:H7 contamination in the last 3+ months.

What is a Class I recall?

A Class I recall, according to FDA definitions, should occur when "there is a reasonable probability that the use of or exposure to a violative product will cause serious adverse health consequences or death."  Class II and III recalls are appropriate only when there is a significantly lesser, or remote, risk of adverse health consequences, or when the health consequences are minor.  Due to its lethal capacity, E. coli O157:H7 is a bacteria that always requires a Class I recall.

What is E. coli O157:H7?

Escherichia coli (E. coli) are members of a large group of bacterial germs that inhabit the intestinal tract of humans and other warm blooded animals (mammals, birds). Newborns have a sterile alimentary tract which within two days becomes colonized with E. coli.

More than 700 serotypes of E. coli have been identified. The different E. coli serotypes are distinguished by their “O” and “H” antigens on their bodies and flagella, respectively. The E. coli serotypes that are responsible for the numerous reports of contaminated foods and beverages are those that produce Shiga toxin (Stx), so called because the toxin is virtually identical to that produced by another bacteria known as Shigella dysenteria type 1 (that also causes bloody diarrhea and hemolytic uremic syndrome [HUS] in emerging countries like Bangladesh) (Griffin & Tauxe, 1991, p. 60, 73). The best known and most notorious Stx-producing E. coli is E. coli O157:H7. It is important to remember that most kinds of E. coli bacteria do not cause disease in humans, indeed, some are beneficial, and some cause infections other than gastrointestinal infections, such urinary tract infections. This section deals specifically with Stx-producing E. coli, including specifically E. coli O157:H7.

Shiga toxin is one of the most potent toxins known to man, so much so that the Centers for Disease Control and Prevention (CDC) lists it as a potential bioterrorist agent (CDC, n.d.). It seems likely that DNA from Shiga toxin-producing Shigella bacteria was transferred by a bacteriophage (a virus that infects bacteria) to otherwise harmless E. coli bacteria, thereby providing them with the genetic material to produce Shiga toxin.

Although E. coli O157:H7 is responsible for the majority of human illnesses attributed to E. coli, there are additional Stx-producing E. coli (e.g., E. coli O121:H19) that can also cause hemorrhagic colitis and post-diarrheal hemolytic uremic syndrome (D+HUS). HUS is a syndrome that is defined by the trilogy of hemolytic anemia (destruction of red blood cells), thrombocytopenia (low platelet count), and acute kidney failure.

Stx-producing E. coli organisms have several characteristics that make them so dangerous. They are hardy organisms that can survive several weeks on surfaces such as counter tops, and up to a year in some materials like compost. They have a very low infectious dose meaning that only a relatively small number of bacteria, less than 50, are needed “to set-up housekeeping” in a victim’s intestinal tract and cause infection.

The Centers for Disease Control and Prevention (CDC) estimates that every year at least 2000 Americans are hospitalized, and about 60 die as a direct result of E. coli infections and its complications. A recent study estimated the annual cost of E. coli O157:H7 illnesses to be $405 million (in 2003 dollars) which included $370 million for premature deaths, $30 million for medical care, and $5 million for lost productivity (Frenzen, Drake, and Angulo, 2005).

What is Hemolytic Uremic Syndrome?

Post-diarrheal Hemolytic Uremic Syndrome (D+HUS) is a severe, life-threatening complication that occurs in about 10% of those infected with E. coli O157:H7 or other Shiga toxin (Stx) producing E. coli. D+HUS was first described in 1955, but was not known to be secondary to E. coli infections until 1982. It is now recognized as the most common cause of acute kidney failure in infants and young children. Adolescents and adults are also susceptible, as are the elderly who often succumb to the disease.

How did these otherwise harmless E. coli become such killers? It seems likely that DNA from a Shiga toxin producing bacterium known as Shigella dysenteriae type 1 was transferred by a bacteriophage (bacteria infected with a virus) to harmless E. coli bacteria, thereby providing them with the genes to produce one of the most potent toxins known to man. So potent, that the Department of Homeland Security lists it as a potential bioterrorist agent. Although E. coli O157:H7 are responsible for the majority of cases in America, there are many additional Stx producing E. coli that can cause D+ HUS.

The chain of events leading to HUS begins with ingestion of Stx producing E. coli (e.g., E. coli O157: H7) in contaminated food, beverages or through person to person transmission. These E. coli rapidly multiply in the intestines causing colitis (diarrhea), and tightly bind to cells that line the large intestine. This snug attachment facilitates absorption of the toxin into the circulation where it becomes attached to weak receptors on white blood cells (WBC) thus allowing the toxin to “ride piggyback” to the kidneys where it is transferred to numerous avid (strong) Gb3 receptors that grasp and hold on to the toxin. Organ injury is primarily a function of Gb3 receptor location and density. Receptors are probably heterogeneously distributed in the major body organs, and this may explain why some patients develop injury in other organs (e.g., brain, pancreas).

Once Stx attaches to receptors, it moves into the cell’s cytoplasm where it shuts down the cells’ protein machinery resulting in cellular injury and/or death. This cellular injury activates blood platelets and the coagulation cascade which results in the formation of clots in the very small vessels of the kidney resulting in acute kidney injury and failure. The red blood cells are hemolyized (destroyed) by Stx and/or damaged as they attempt to pass through partially obstructed microvessels. Blood platelets (required for normal blood clotting), are trapped in the tiny blood clots or are damaged and destroyed by the spleen.