The Bakersfield Californian reported today that at least four children have become ill with symptoms of E. coli infection, and have been hospitalized – two with hemolytic uremic syndrome (HUS). Health officials are continuing their investigation into the apparent outbreak, and are assessing potential common exposures the children may have had. According to the article, "At this point, all that’s known is that the four children, who know one another from school or play dates, suffered bloody diarrhea after attending several parties and playing at a local park."
KGET reported that seven children had been counted as being part of the potential outbreak:
[S]ix kindergardners are sick, some of them hospitalized with the sometimes fatal disease.
An eighth student is a 10-year-old relative of of one of the kindergarders.
HUS develops when the toxin from E. coli bacteria, known as Shiga-like toxin (SLT) [1,2], enters the circulation by binding to special receptors. These Shiga-toxin receptors, known as Gb3 receptors [1], are probably heterogeneously distributed in the major body organs allowing disparate thrombotic (blood clotting) impacts in different HUS victims, although the greatest receptor concentration appears to be in the kidneys, especially in children. As the inflammatory reaction process accelerates, red blood cells are destroyed and cellular debris aggregates within the microvasculature while the body’s inherent clot breaking mechanisms are disrupted. The result is formation of microthrombi within particularly susceptible organs such as the kidneys and brain. Because there exists no way to halt the progression of HUS, doctors are left to support the HUS victim while the acute process runs its course.
Some organs appear more susceptible than others to the damage caused by these toxins, possibly due to the presence of increased numbers of toxin-receptors. These organs include the kidney, pancreas, and brain. An animated video of how E. coli attaches to the intestinal wall and releases shiga-toxins, causing infection, is available at the Howard Hughes Medical Institute Web site.
[1] Recent research suggests that E. coli O157:H7 acquired its pathological character when a bacteriophage (virus that infects bacteria) transmitted genetic material for the creation of the toxin from a closely related Shigella bacterial species (hence the epithet, Shiga-like toxin) to a formerly benign species of E. coli.
[2] Verotoxin-globotriaosyl ceramide binding receptors.