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
EHEC (enterohemorrhagic E. coli): bloody diarrhea,
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
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
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