A 4 year old girl is now fighting for her life after contracting E. coli O157:H7 and developing HUS after attending a July 3 picnic hosted by Neff’s Lawn Care in Germantown, Ohio. As reported today by Peggy O’Farrell at the Dayton Daily News, the little girl is currently in critical condition at an undisclosed hospital. Thus far 63 people have been sickened in this outbreak, with 11 now culture-confirmed with the same bacterial strain, E. coli O157:H7.
Public health officials with Montgomery and Dayton Counties are currently interviewing those who attended the picnic and became ill to try and pinpoint the exact source of the bacterial contamination.
Hemolytic Uremic Syndrome (HUS), occurs in approximately 10% of those who become infected with E. coli O157:H7 or similar Shiga toxin-producing E. coli.
The chain of events leading to HUS begins with the ingestion of Shiga toxin-producing E. coli—for example, E. coli O157: H7—in contaminated food or beverages, or as a result of exposure to animals carrying the bacteria, or from 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, thus allowing the toxin to “ride piggyback” to the kidneys where it is transferred to numerous avid (strong) Gb3 receptors that grasp and then hold on to the toxin.
Organ injury is primarily a function of receptor location and density. The receptors are probably diversely distributed in the major body organs, and this may explain why some patients develop injury in different organs—for example, the brain or pancreas.
Once the Shiga toxins attach to receptors, they move into the interior of the cell (cytoplasm), where the toxins shut down the protein machinery, resulting in cellular injury or death. Injury activates blood platelets and the “coagulation cascade.” This coagulation causes the formation of clots in the very small vessels of the kidney, resulting in acute kidney injury and failure.
The red blood cells are either destroyed by the Shiga toxin (hemolytic destruction), or they are damaged as the cells attempt to pass through partially obstructed microvessels. Blood platelets, which are required for normal blood clotting, become trapped in the tiny blood clots, or they are damaged and destroyed by the spleen.