Reese's Playroom Inc.

HUS accounts for the majority of the acute deaths and chronic injuries caused by the bacteria. [3] HUS occurs in 2-7% of victims, primarily children, with onset five to ten days after diarrhea begins. [23, 44] “E. coli serotype O157:H7 infection has been recognized as the most common cause of HUS in the United States, with 6% of patients developing HUS within 2 to 14 days of onset of diarrhea.” [44, 45] And it is the most common cause of renal failure in children. [26, 45, 48] 

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Approximately half of the children who suffer HUS require dialysis, and at least 5% of those who survive have long term renal impairment. [44] The same number suffers severe brain damage. [46]  While somewhat rare, serious injury to the pancreas, resulting in death or the development of diabetes, also occurs. [47] There is no cure or effective treatment for HUS. [47] And, tragically, children with HUS too often die, with a mortality rate of five to ten percent. [26]

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Once Shiga toxins attach to receptors on the inside surface of blood vessel cells (endothelial cells), a chemical cascade begins that results in the formation of tiny thrombi (blood clots) within these vessels. [33, 45]  Some organs seem more susceptible, perhaps due to the presence of increased numbers of receptors, and include the kidney, pancreas, and brain. [26, 33]  Consequently, organ injury is primarily a function of receptor location and density. [33, 54]

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Once they move into the interior of the cell (cytoplasm), Shiga toxins shut down protein machinery, causing cellular injury or death. [33, 46] This cellular injury activates blood platelets too, and the resulting “coagulation cascade” causes the formation of clots in the very small vessels of the kidney, leading to acute kidney failure.

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The red blood cells are either directly destroyed by Shiga toxin (hemolytic destruction), or are damaged as cells attempt to pass through partially obstructed micro-vessels. [33, 46] Blood platelets become trapped in the tiny blood clots, or they are damaged and destroyed by the spleen. [46]

By definition, when fully expressed, HUS presents with the triad of hemolytic anemia (destruction of red blood cells), thrombocytopenia (low platelet count), and renal failure (loss of kidney function). [33, 45] Although recognized in the medical community since at least the mid-1950s, HUS first captured the public’s widespread attention in 1993 following a large E. coli outbreak in Washington State that was linked to the consumption of contaminated hamburgers served at a fast-food chain. [6, 28] Over 500 cases of E. coli  were reported; 151 were hospitalized (31%), 45 persons (mostly children) developed HUS (9%), and three died. [6, 28]

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Of those who survive HUS, at least five percent will suffer end stage renal disease (ESRD) with the resultant need for dialysis or transplantation. [47]  But, “because renal failure can progress slowly over decades, the eventual incidence of ESRD cannot yet be determined.” [33]  Other long-term problems include the risk for hypertension, proteinuria (abnormal amounts of protein in the urine that can portend a decline in renal function), and reduced kidney filtration rate. [33, 47]  Since the longest available follow-up studies of HUS victims are 25 years, an accurate lifetime prognosis is not really available and remains controversial. [47] 

You can read more about HUS at About-HUS.com. 

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Other Complications from E. coliInfection

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IBS is a chronic disorder characterized by alternating bouts of constipation and diarrhea, both of which are generally accompanied by abdominal cramping and pain. [50] Suffering an E. coli O157:H7 infection has been linked to the development of post-infectious irritable bowel syndrome (IBS).  This link was demonstrated by the Walkerton Health Study (WHS), which followed one of the largest O157:H7 outbreaks in the history of North America. [49] In this outbreak, contaminated drinking water caused over 2,300 people to be infected, resulting in 27 recognized cases of HUS, and 7 deaths. The WHS followed 2,069 eligible study participants. Among its findings, WHS noted that, “Between 5% and 30% of patients who suffer an acute episode of infectious gastroenteritis develop chronic gastrointestinal symptoms despite clearance of the inciting pathogens.” [49]

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Not surprisingly, E. coli O157:H7 infection is associated with long-term emotional disruption as well, not just for the victim, but for entire families. [51]  A recent study reported that “parents experienced long-term emotional distress and substantive disruption to family and daily life” following an E. coli O157:H7 infection in the family. [51]