Dr. Charles "Pat" Davis, MD, PhD, is a board certified Emergency Medicine doctor who currently practices as a consultant and staff member for hospitals. He has a PhD in Microbiology (UT at Austin), and the MD (Univ. Texas Medical Branch, Galveston). He is a Clinical Professor (retired) in the Division of Emergency Medicine, UT Health Science Center at San Antonio, and has been the Chief of Emergency Medicine at UT Medical Branch and at UTHSCSA with over 250 publications.
Jay W. Marks, MD, is a board-certified internist and gastroenterologist. He graduated from Yale University School of Medicine and trained in internal medicine and gastroenterology at UCLA/Cedars-Sinai Medical Center in Los Angeles.
The major symptom that all enterovirulent E. coli (EEC) produce in common is diarrhea; these organisms are the leading cause of bacterial gastroenteritis. However, the type of diarrhea (for example, bloody, chronic, or self-limiting) and the complications that may accompany the infections differ somewhat from each other. These symptoms have caused researchers and clinicians to arrange E. coli serotypes into groups according to their different symptoms and disease causing (pathogenic) mechanisms. Depending on which research or clinical physicians publications are read, there are 4 to 6 groups of E. coli that comprise all of the enterovirulent E. coli (EEC). Unfortunately, some investigators have more than one term for some members of the groups. The following is a summary of the groups that are currently in the literature and the symptoms E. coli group members cause:
EHEC (enterohemorrhagic E. coli): bloody diarrhea, hemorrhagic colitis, hemolytic uremic syndrome (HUS), and thrombotic thrombocytopenic purpura (TTP); additional terms for EHEC are VTEC and STEC which stand for Vero toxin-producing E. coli and Shiga toxin-producing E. coli, respectively. One serotype, E. coli 0157:H7, is responsible for the majority of the bloody diarrhea that occurs due to the production of Shiga toxins.
ETEC (enterotoxigenic E. coli):traveler's diarrhea, a watery diarrhea with nausea, abdominal cramping, and fever, caused by several serotypes of E. coli (0169:H47, 0148:H28 and several others) that produce two toxins that cause the gastrointestinal tract to secrete fluid (secretory exotoxins)
EPEC (enteropathogenic E. coli): childhood diarrhea, caused by E. coli bacteria (many different serotypes) that can attach to gastrointestinal tissues, especially in infants, and produces a watery or bloody diarrhea in infants by producing a toxin similar to that produced by the bacterium named Shigella dysenteriae.
EIEC (enteroinvasive E. coli):Shigella-like dysentery with blood and mucus, due to E. coli that invade epithelial cells of people of all ages, also producing vomiting, fever and chills. These serotypes are closely related to Shigella spp. (a few children develop HUS)
EAEC (enteroadherent E. coli): childhood watery diarrhea, some cases of traveler's diarrhea in adults, and some urinary tract infections. This group is composed of E. coli strains (for example, 0119 or 055) that are able to adhere to human cells (gastrointestinal and other cell types). About one-half of this group is able to cause mild diarrhea, usually in children, while other E. coli serotypes that can adhere, do not cause any disease. Like EAggEC, these enteroadherent E. coli do not produce any Shiga toxins or secretory-causing exotoxins.
EAggEC (enteroaggregative E. coli): persistent diarrhea in developing countries especially in children that usually lasts more than 14 days. The diarrhea is watery, mucus-containing, and in about one-third of individuals, bloody. Those with EAggEC usually have only a low fever (less than 101 F or 38.3 C) and almost no vomiting. These E. coli serotypes (for example, 042 and 044) do not produce any Shiga toxins or secretory exotoxins that cause secretions but cause intestinal inflammation that is linked to abnormally high intestinal secretion that leads to watery diarrhea. These strains are unique because they "aggregate" (form small masses comprised of cultured tissue cells and bacteria) human gastrointestinal cells by attaching via fimbriae (pili).
As one can surmise, there are unfortunate overlaps in disease syndromes and that is one reason that authors disagree on the actual number of groups (EPEC, EAEC, and EAggEC or EACE and EAggEC are often lumped together). It seems unlikely that the group names will remain stable in the future (see next section).