Escherichia coli (ETEC) is a Gram-negative,
rod-shaped bacterium that causes
traveler's diarrhea (Figure
1). ETEC bacteria are motile facultative anaerobes
(they can makes ATP energy by aerobic
respiration if oxygen is present, but is also
capable of switching to fermentation) that can easily be
cultured under aerobic conditions at 37°C.
Normally, E. coli serves a useful
function in the body by suppressing the growth
of harmful bacterial species in the small
intestine, and by synthesizing appreciable
amounts of vitamins. However, this particular
strain leads to a major cause of diarrheal
disease in underdeveloped nations that lack
sanitation infrastructure, especially among
with other strains). What differentiates the
various strains of E. coli is when the
bacteria carries an extra piece of genetic
information encoded on a plasmid that, when
translated into a protein, produces toxic
effects on the host. The toxins and the diseases
that ETEC causes are not related to
E. coli O157:H7.
This scanning electron micrograph reveals some
of the morphologic details displayed by two
joined Gram-negative Enterotoxigenic
Escherichia coli (0:169 H41) bacteria
dividing by binary fission [22409 X].
Infection: ETEC is able to infect its
host using a number of virulence
factors, including adhesion proteins
(fimbrial adhesins) that adhesins mediate the
attachment of bacteria to the surface of host
epithelium cells and allow bacterial
colonization, and the production of toxins
(Zhang et al., 2006). In pigs, ETEC
strains that produce adhensins are the most
common currently associated with diarrheal
diseases. These fimbriae bind to glycoconjugates
on enterocytes (intestinal cells), and the
absence of the respective glycoconjugate renders
the animal resistant to bacterial colonization
and consequent diarrheal diseases.
one or both of two potent enterotoxins, namely, heat-labile
(LT) and heat-stable (ST) toxin. Both toxins,
specifically LT, are similar in structure and
function to cholera toxin.
As such, they have been found to disrupt
intestinal fluid homeostasis and to cause
hypersecretion of fluid and electrolytes through
activation of adenylate cyclase (by LT) or
guanylate cyclase (by ST) in small intestinal
mucosal cells (Zhang et al., 2006).
This mechanism elevates either cyclic
AMP or cyclic GMP levels in intestinal
epithelial cells, stimulate
active chloride secretion, inhibit
chloride absorption in the intestinal
epithelium, and subsequently cause
unidirectional fluid secretion (diarrhea). LT is highly immunogenic, but lacks
toxicity. Consequently, it is used in current
vaccines against ETEC. Heat-stable
toxin (ST) is a small peptide
that causes secretion of fluids and
electrolytes, but it lacks immunogenicity
(Rosales-Mendoza et al., 2009). Between
the two, the effect of LT on the host is
substantially greater than that of ST (Zhang
et al., 2006).
Treatment: Most infections
caused by ETEC bacteria are self-limiting
and do not require anti-microbial treatment due
to the short duration
of symptoms; thus, the infection will end on its
own and is rarely life-threatening. Most cases
of the infection arise from
contamination of water used for
drinking and food preparation with fecal matter.
Developed countries with proper sanitation have
a much lower incidence of ETEC infection (Devasia
al., 2006). A lack of proper food sanitation techniques
and allowing a meal to remain unrefrigerated for
hours allows what may have
been a insignificant amount
of contamination to multiply to dangerous levels. Treatment of an
ETEC infection is limited to supportive care
and, more importantly, oral rehydration to replace
fluids lost from diarrhea.
Identification of ETEC from a
stool sample culture is difficult, since it cannot be distinguished from
that is native to the gastrointestinal
tract. When stool
cultures do not show a routine enteric pathogen,
symptoms may be attributed
to a viral cause without confirmatory tests
al., 1999). Because further
testing would extend after symptoms have
subsided, it is not usually pursued.
Biochemical and serotyping methods are typically
used for identification of
bacterial pathogens (Stenutz et al., 2006). Serotyping to identify
ETEC is not useful as the level of detail
required is beyond the scope of most
laboratories. Recall that in some cases, what
differentiates a nonpathogenic E. coli
bacterium from a pathogen one is a difference in
genomic material. Serotyping
identification of E. coli is based
on somatic, flagellar, and capsular surface
antigen profiles (Stenutz et al.,
The most used methods for the identification of enterotoxigenic strains are
polymerase chain reaction to test for the
presence of the genes encoding the
heat-stable and heat-labile toxins (estA
eltA (LT)) and assays for the detection
of the toxins (Stenutz et
Dalton, C.B., Mintz, E.D.,
Wells, J.G., Bopp, C.A. & Tauxe, R.V. (1999).
Outbreaks of enterotoxigenic
Escherichia coli infection in America adults: a
clinical and epidemiologic profile. Epidemiology
and Infection, 123: 9-16.
Devasia, R.A., Jones, T.F., Ward, J., Stafford,
L., Hardin, H., Bopp, C., Beatty, M., Mintz, E.
& Schaffner, W. (2006). Endemically Acquired Foodborne
Outbreak of Enterotoxin-producing Escherichia coli Serotype O169:H41.
Journal of Medicine, 119: 6-10.
Rosales-Mendoza, S., Alpuche-Solis, A.G., Soria-Guerra,
R.E., Moreno-Fierros, L., Martinez-Gonzalez, L.,
Herrera-Diaz, A. & Korban, S.S. (2009).
Expression of an Escherichia coli antigenic
fusion protein comprising the heat labile toxin
B subunit and the heat stable toxin, and its
assembly as a functional oligomer in
transplastomic tobacco plants. The Plant Journal,
Stenutz, R., Weintraub, A. and Widmalm, G.
structures of Escherichia coli Opolysaccharide
antigens. FEMS Microbiology Reviews, 30:
Zhang, E.M., Berberov, J.F.,
et al. (2006). Significance of
Heat-Stable and Heat-Labile Enterotoxins in
Porcine Colibacillosis in an Additive Model for
Pathogenicity Studies. Infection and
Immunity, 74(6): 3107-3114.