Oklahoma is recovering from an outbreak of Escherichia coli which has kept me away from the blog recently.
E. coli, as we usually call it, lives all around and in us. A good chunk of that microbiome we keep hearing about includes this bacteria. Most strains happily thrive in our guts, living a perfectly benign coexistence with us. At times they may find their way into our urine or other problematic place, but they can usually be rapidly dispatched.
Some strains produce a toxin first noted in the bacteria Shigella, thus named Shiga Toxin. Autocorrect on my iPhone wants to change "shiga" to "shiva." This may not be an error. This toxin causes incredible inflammation within the bowel. When the gut gets inflamed, it lets water and other material flow on through, producing diarrhea. In this case, the inflammation is so intense that the gut bleeds. A bloody gut produces bloody diarrhea. Nausea, vomiting, and intense cramping complete the clinical picture. This is a case of the runs you will never forget.
In a small number of cases of hemorrhagic colitis, the toxin enters the blood stream and produces a systemic response called a thrombotic microangiopathy (TMA for short). In tiny blood vessels throughout the body (capillaries), the toxin damages the inside. Platelets (oblong lavender thingies in the diagram) activate on these areas of damage to begin repairs. These tiny clots get bigger over time and form a mesh or halt blood blow to an organ, impairing or shutting down its function.
Not all organs seem as prone to TMA damage. The kidneys seem to provide a playground for the toxin and platelets; kidney involvement ranges from the trivial to irreversible infarction or scarring of the kidneys. This is why we call this TMA hemolytic uremic syndrome (HUS), uremia being another term for kidney failure. Other organs can be involved, including the brain, pancreas, liver, and heart.
Obviously the kidney provides a major clotting magnet, or I would not be discussing this entity. We do not really know why one child gets colitis and develops HUS while another gets just a horrible case of diarrhea. Using antibiotics and anti-diarrheal drugs during the colitis can increase the risk of HUS, but they do not explain it all.
Since this syndrome was described in the 1950's mortality has fallen from ~50% to <5% just with supportive care. Mortality generally is confined to patients with significant central nervous system involvement. Apparent kidney recovery occurs in 95% of survivors, although most will develop other signs and symptoms of chronic kidney disease over the decades.