Last night we learned that a 5-year-old Indiana girl died from an E. coli infection while hospitalized at Riley Children’s Hospital in Indianapolis. It is almost certain that she was suffering from the devastating effects of hemolytic uremic syndrome, or HUS, which is caused by the toxins that many strains of E. coli, including E. coli O157:H7, release in the gastrointestinal tract. (More on HUS below)
Faith Baptist Church Senior Pastor Marc Monte said the 5-year-old girl’s family lives in Hendricks County, Indiana. Kalei Welch’s parents are working with Indiana health officials to try to pinpoint the exact source of her E. coli infection. Although a source has not been determined, press reports indicate that Kalei may have attended a fair in the days before the onset of her E. coli illness. County health officials indicate, however, that they have not received any other reports of illness amongst patrons of the fair.
There are many possible answers to the question where Kalei was infected, especially during these summer months. Indiana’s top-tier public health and medical system are undoubtedly working hard on the case.
It is, however, sadly ironic timing for Kalei’s passing. Today two of our attorneys are in North Carolina delivering opening statements in a trial concerning the 2004 E. coli O157:H7 outbreak at the North Carolina State Fair petting zoo. We represent a number of children sickened in that outbreak who developed HUS. Read Bill Marler’s warnings on the dangers of petting zoos at fairs at Petting Zoos – Still Dangerous – E. coli O157:H7.
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, animal to person, or person-to-person transmission.
These E. coli rapidly multiply in the intestine causing colitis (diarrhea), and tightly bind to cells that line the large intestine. This snug attachment facilitates absorption of the toxin into the intestinal capillaries and into the systemic 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 undergo hemolytic destruction by Stx and/or damage 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.