Shortly after I resolved the 1996 Odwalla E. coli O157:H7 outbreak on behalf of five kids that suffered Hemolytic Uremic Syndrome (HUS), and long before Google became synonymous with searching on the Internet, we had compiled more information about this nasty bug, and its frightening and potentially deadly impact, than anyone outside a few major teaching hospitals.

After I started Marler Clark in 1998 along with Bruce Clark, Denis Stearns and Andy Weisbecker, E. coli O157:H7 cases – especially those linked to ground beef – arrived at our offices at a far too frequent rate.  So too came the calls and questions from media trying to understand what was happening to kids and the All-American hamburger.

For those who do not recall Prodigy or Netscape, in 1998 few could envision that the Internet would be more than a place to park what in essence were online Word documents.  So, in early 1999 we placed everything we knew about E. coli O157:H7 and HUS on and  The idea was when someone called you would direct them to the site to read for themselves about the dangers of E. coli O157:H7 and HUS.  I think few at the time – certainly not me – thought that people would search for these things for themselves by using “search terms.”

Over the years both sites have gone through substantive changes – both in content quality and look.  We have had the opportunity and honor to work with the best pediatric nephrologists in the world, and the patients they cared for.  In the last month both sites have undergone edited content and an updated look – here are the highlights:

E. coli

Escherichia coli (or E. coli) is the most prevalent infecting organism in the family of gram-negative bacteria known as enterobacteriaceae.  E. coli bacteria were discovered in the human colon in 1885 by German bacteriologist Theodor Escherich.  Dr. Escherich also showed that certain strains of the bacterium were responsible for infant diarrhea and gastroenteritis, an important public health discovery. Although E. coli bacteria were initially called Bacterium coli, the name was later changed to Escherichia coli to honor its discoverer.

E. coli is often referred to as the best or most-studied free-living organism.  More than 700 serotypes of E. coli have been identified.  The “O” and “H” antigens on the bacteria and their flagella distinguish the different serotypes.  It is important to remember that most kinds of E. coli bacteria do not cause disease in humans.  Indeed, some E. coli are beneficial, while some cause infections other than gastrointestinal infections, such as urinary tract infections.

The E. coli that are responsible for the numerous reports of contaminated foods and beverages are those that produce Shiga toxin, so called because the toxin is virtually identical to that produced by Shigella dysenteria type 1.  The best-known and also most notorious E. coli bacteria that produce Shiga toxin is E. coli O157:H7.  The Centers for Disease Control and Prevention (CDC) has estimated that every year at least 2,000 Americans are hospitalized, and about 60 die as a result of E. coli infection and its complications.

E. coli are classified by their O and H antigens (e.g., E. coli O157:H7, E. coli O26:H11) and broadly categorized as Shiga toxin-producing E. coli (STEC) O157 or non-O157 STEC.  For many years, most recognized STEC outbreaks were associated with STEC O157. Despite the dominance of STEC O157, at least 150 non-O157 strains of E. coli are known to cause human illness and have been associated with outbreaks.

In the US, documented outbreaks of non-O157 E. coli include 10 involving O111; 6 involving O26; 3 involving O45; 2 involving O145, O104, and O6; and, one each involving O51; O103; O27; and, O84. Non-O157 STEC outbreaks are rare, but tend to primarily be due to contaminated food and person-to-person transmission.

In recent years, improved diagnostic assays for non-O157 STEC have contributed to an increased appreciation of the severity of disease caused by these strains, including hemolytic uremic syndrome (HUS).  Notably, the number of non-O157 STEC cases reported to CDC’s FoodNet has risen steadily each year; from 2000-2006, there was an overall 4-fold increase in incidence (0.12 cases per 100,000 to 0.42 cases per 100,000 population) at FoodNet sites. The most common serogroups reported to cause foodborne illness in the United States are O26, O111, O103, O121, O45, and O145.  These six serotypes account for 75% of human infections.

Worldwide, non-O157 STEC outbreaks emerged in the 1980s, and the first reported outbreaks in the United States occurred in the 1990s.  The number of reported outbreaks due to non-O157 STECs remains relatively low in the United States, but experts agree that documented outbreaks probably represent the “tip of the iceberg.”  From 1983-2002, seven non-O157 STEC outbreaks were reported in the United States.  During the following five-year period from 2003-2007, CDC documented an additional five non-O157 STEC outbreaks (CDC Outbreak Surveillance Data.  A study of non-O157 STEC concluded that these strains may account for up to 20 to 50% of all STEC infections in the United States.

For more on E. coli, visit

Hemolytic Uremic Syndrome

Post-diarrheal Hemolytic Uremic Syndrome is a severe, life-threatening complication that occurs in about 10% of those infected with Escherichia coli (E. coli) O157:H7 or other Shiga toxin-producing E. coli.

Post-diarrheal HUS is usually signified as “D+ HUS,” while HUS not preceded by diarrhea is signified as “D- HUS.”  (For the ease of reference, we will use HUS throughout this site unless some more specific terminology is needed.)

HUS was first described in 1955, but was not known to be secondary to E. coli infections until 1982.  It is now recognized as the most common cause of acute kidney failure in infants and young children.  Adolescents and adults are also susceptible, as are the elderly, who often die as a result of the disease.

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.

For more on Hemolytic Uremic Syndrome, visit