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Tag words: Escherichia coli, E. coli, E. coli O157:H7, enteropathogenic E. coli, EPEC, enterotoxigenic E. coli, ETEC, LT toxin, ST toxin, vero toxin, shiga toxin, food poisoning, gastroenteritis, hemolytic uremic syndrome, HUS, neonatal meningitis, urinary tract infection, UTI.

Escherichia coli

Kingdom: Bacteria
Phylum: Proteobacteria
Class: Gamma Proteobacteria
Order: Enterobacteriales
Family: Enterobacteriaceae
Genus: Escherichia
Species: E. coli

Kenneth Todar currently teaches Microbiology 100 at the University of Wisconsin-Madison.  His main teaching interest include general microbiology, bacterial diversity, microbial ecology and pathogenic bacteriology.

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Pathogenic E. coli (page 4)

(This chapter has 4 pages)

© Kenneth Todar, PhD

Intestinal Diseases Caused by E. coli

As a pathogen, E. coli is best known for its ability to cause intestinal diseases. Five classes (virotypes) of E. coli that cause diarrheal diseases are now recognized: enterotoxigenic E. coli (ETEC), enteroinvasive E. coli (EIEC), enterohemorrhagic E. coli (EHEC), enteropathogenic E. coli (EPEC), and enteroaggregative E. coli (EAEC). Each class falls within a serological subgroup and manifests distinct features in pathogenesis. A summary of the characteristics of diarrheagenic strains of E. coli is given in Table 2 at the end of this article.

Enterotoxigenic E. coli (ETEC)

ETEC is an important cause of diarrhea in infants and travelers in underdeveloped countries or regions of poor sanitation. In the U.S., it has been implicated in sporadic waterborne outbreaks, as well as due to the consumption of soft cheeses, Mexican-style foods and raw vegetables. The diseases vary from minor discomfort to a severe cholera-like syndrome. ETEC are acquired by ingestion of contaminated food and water, and adults in endemic areas evidently develop immunity. The disease requires colonization and elaboration of one or more enterotoxins. Both traits are plasmid-encoded.

ETEC may produce a heat-labile enterotoxin (LT) that is similar in molecular size, sequence, antigenicity, and function to the cholera toxin (Ctx). It is an 86kDa protein composed of an enzymatically active (A) subunit surrounded by 5 identical binding (B) subunits. It binds to the same identical ganglioside receptors that are recognized by the cholera toxin (i.e., GM1), and its enzymatic activity is identical to that of the cholera toxin.

ETEC may also produce a heat stable toxin (ST) that is of low molecular size and resistant to boiling for 30 minutes. There are several variants of ST, of which ST1a or STp is found in E. coli isolated from both humans and animals, while ST1b or STh is predominant in human isolates only. The ST enterotoxins are peptides of molecular weight about 4,000 daltons. Their small size explains why they are not inactivated by heat. ST causes an increase in cyclic GMP in host cell cytoplasm leading to the same effects as an increase in cAMP. ST1a is known to act by binding to a guanylate cyclase that is located on the apical membranes of host cells, thereby activating the enzyme. This leads to secretion of fluid and electrolytes resulting in diarrhea.

The infective dose of ETEC for adults has been estimated to be at least 108 cells; but the young, the elderly and the infirm may be susceptible to lower numbers.

ETEC adhesins are fimbriae which are species-specific. For example, the K-88 fimbrial Ag is found on strains from piglets; K-99 Ag is found on strains from calves and lambs; CFA I, and CFA II, are found on strains from humans. These fimbrial adhesins adhere to specific receptors on enterocytes of the proximal small intestine.

Symptoms ETEC infections include diarrhea without fever. The bacteria colonize the GI tract by means of a fimbrial adhesin, e.g. CFA I and CFA II, and are noninvasive, but produce either the LT or ST toxin. <>

Enteroinvasive E. coli (EIEC)

EIEC closely resemble Shigella in their pathogenic mechanisms and the kind of clinical illness they produce. EIEC penetrate and multiply within epithelial cells of the colon causing widespread cell destruction. The clinical syndrome is identical to Shigella dysentery and includes a dysentery-like diarrhea with fever. EIEC apparently lack fimbrial adhesins but do possess a specific adhesin that, as in Shigella, is thought to be an outer membrane protein. Also, like Shigella, EIEC are invasive organisms. They do not produce LT or ST toxin.

There are no known animal reservoirs of EIEC. Hence the primary source for EIEC appears to be infected humans. Although the infective dose of Shigella is low (in the range of 10 to few hundred cells), volunteer feeding studies showed that at least 106 EIEC organisms are required to cause illness in healthy adults. Unlike typical E. coli, EIEC are non-motile, do not decarboxylate lysine and do not ferment lactose. Pathogenicity of EIEC is primarily due to its ability to invade and destroy colonic tissue. The invasion phenotype, encoded by a high molecular weight plasmid, can be detected by PCR and probes for specific for invasion genes.

Enteropathogenic E. coli (EPEC)

EPEC induce a profuse watery, sometimes bloody, diarrhea. They are a leading cause of infantile diarrhea in developing countries. Outbreaks have been linked to the consumption of contaminated drinking water as well as some meat products.  Pathogenesis of EPEC involves a plasmid-encoded protein referred to as EPEC adherence factor (EAF) that enables localized adherence of bacteria to intestinal cells and a non fimbrial adhesin designated intimin, which is an outer membrane protein that mediates the final stages of adherence. They do not produce ST or LT toxins.

Adherence of EPEC strains to the intestinal mucosa is a very complicated process and produces dramatic effects in the ultrastructure of the cells resulting in rearrangements of actin in the vicinity of adherent bacteria. The phenomenon is sometimes called "attachment and effacing" of cells. EPEC strains are said to be "moderately-invasive",  meaning they are not as invasive as Shigella, and unlike ETEC or EAEC, they cause an inflammatory response. The diarrhea and other symptoms of EPEC infections probably are caused by bacterial invasion of host cells and interference with normal cellular signal transduction, rather than by production of toxins.

Through volunteer feeding studies the infectious dose of EPEC in healthy adults has been estimated to be 106 organisms.

Some types of EPEC are referred to as diffusely adherent E. coli (DAEC), based on specific patterns of adherence. They are an important cause of traveler's diarrhea in Mexico and in North Africa.

Enteroaggregative E. coli (EAEC)

The distinguishing feature of EAEC strains is their ability to attach to tissue culture cells in an aggregative manner. These strains are associated with persistent diarrhea in young children. They resemble ETEC strains in that the bacteria adhere to the intestinal mucosa and cause non-bloody diarrhea without invading or causing inflammation. This suggests that the organisms produce an enterotoxin of some sort. Recently, a distinctive heat-labile plasmid-encoded toxin has been isolated from these strains, called the EAST (EnteroAggregative ST) toxin. They also produce a hemolysin related to the hemolysin produced by E. coli strains involved in urinary tract infections. The role of the toxin and the hemolysin in virulence has not been proven. The significance of EAEC strains in human disease is controversial.

Enterohemorrhagic E. coli (EHEC)

EHEC are recognized as the primary cause of hemorrhagic colitis (HC) or bloody diarrhea, which can progress to the potentially fatal hemolytic uremic syndrome (HUS). EHEC are characterized by the production of verotoxin or Shiga toxins (Stx). Although Stx1 and Stx2 are most often implicated in human illness, several variants of Stx2 exist.

There are many serotypes of Stx-producing E. coli , but only those that have been clinically associated with HC are designated as EHEC. Of these, O157:H7 is the prototypic EHEC and most often implicated in illness worldwide. The infectious dose for O157:H7 is estimated to be 10 - 100 cells; but no information is available for other EHEC serotypes. EHEC infections are mostly food or water borne and have implicated undercooked ground beef, raw milk, cold sandwiches, water, unpasteurized apple juice and vegetables

EHEC are considered to be "moderately invasive". Nothing is known about the colonization antigens of EHEC but fimbriae are presumed to be involved. The bacteria do not invade mucosal cells as readily as Shigella, but EHEC strains produce a toxin that is virtually identical to the Shiga toxin. The toxin plays a role in the intense inflammatory response produced by EHEC strains and may explain the ability of EHEC strains to cause HUS. The toxin is phage encoded and its production is enhanced by iron deficiency.

E. coli O157:H7 Transmission EM. American Society for Microbiology

Table 2. Diarrheagenic E. coli: virulence determinants and characteristics of disease
fimbrial adhesins e.g. CFA I, CFAII, K88. K99
non invasive
produce LT and/or ST toxin
watery diarrhea in infants and travelers; no inflammation, no fever


nonfimbrial adhesins, possibly outer membrane protein
invasive (penetrate and multiply within epithelial cells)
does not produce shiga toxin
dysentery-like diarrhea (mucous, blood), severe inflammation, fever

non fimbrial adhesin (intimin)
EPEC adherence factor (EAF) enables localized adherence of bacteria to intestinal cells
moderately invasive (not as invasive as Shigella or EIEC)
does not produce LT or ST; some reports of shiga-like toxin
usually infantile diarrhea; watery diarrhea with blood, some inflammation, no fever; symptoms probably result mainly from invasion rather than toxigenesis

adhesins not characterized
non invasive
produce ST-like toxin (EAST) and a hemolysin
persistent diarrhea in young children without inflammation or fever

adhesins not characterized, probably fimbriae
moderately invasive
does not produce LT or ST but does produce shiga toxin
pediatric diarrhea, copious bloody discharge (hemorrhagic colitis), intense inflammatory response, may be complicated by hemolytic uremia


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Kenneth Todar has taught microbiology to undergraduate students at The University of Texas, University of Alaska and University of Wisconsin since 1969.

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