WISHTV.com reports that two Rush County Indiana children are in critical children after contracting E. coli infections.  Almost certainly these two children are suffering from hemolytic uremic syndrome, or HUS.  There is some suspicion that the two children may have become infected at the Rush County Fair petting zoo in late June, although the proof of that link is not clear based on the reports. 

According to WISH TV:

Kathleen Ragan, 4, is at the Peyton Manning Children’s Hospital suffering from Hemolytic Uremic Syndrome. "With the HUS, her kidneys have still not started functioning correctly," says Kathleen’s mother, Angel Campbell-Ragan. "She’s still on the dialysis."

Kathleen’s mother says she did use hand sanitizer as she petted animals there, but her symptoms of fatigue, diarrhea and bloody stools started the day after the fair ended.

The parent of at least one other Rush County child said that her boy is also suffering from HUS, but he wasn’t at the fair. 

About hemolytic uremic syndrome

The chain of events leading to HUS begins with ingestion of shiga toxin producing E. coli (including E. coli O157:H7) in contaminated food, beverages, person to person, or animal 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.