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et al., 2009
). Given the genomic diversity of ETEC, and the complex interac-
tions between these organsims and the host, it is likely that there are many such
human polymorphisms that might predispose to development (or prevention)
of symptomatic ETEC infections. These would include mutations in innate
immune effector molecules that control ETEC, as exemplified by the identifica-
tion of single-nucleotide polymorphisms (SNPs) in the human lactoferrin gene
among travelers with symptomatic ETEC infection (
Mohamed et al., 2007
), as
well as SNPs in CD14, a lipopolysaccharide receptor that is induced in travelers'
diarrhea (
Mohamed et al., 2011
). Interestingly, polymorphisms associated with
higher levels of interleukin (IL-10), an anti-inflammatory cytokine, have been
associated with an increased risk of symptomatic ETEC infection (
Flores et al.,
2008
).
Complications
The most common serious complication of ETEC diarrhea is profound dehy-
dration. Particularly among young children, ETEC and rotavirus contribute
disproportionately to episodes of life-threating dehydration in developing coun-
tries (
Black et al., 1981
). Similarly, among older children and adults in low- and
middle-income countries, two groups of pathogens, ETEC and
Vibrio cholerae,
are most frequently associated with severe illness requiring hospitalization
(
Fischer Walker et al., 2010
).
Another more pernicious but important effect of diarrheal illness attributed to
ETEC is childhood stunting (
Ricci et al., 2006
;
Mondal et al., 2009, 2012
). The
relationship between infectious diarrheal illnesses and malnutrition is complex,
with multiple studies implicating diarrhea caused by ETEC and other pathogens
as a cause and a consequence of malnutrition (
Guerrant et al., 1992
;
Mondal
et al., 2012
). Repeated bouts of diarrhea in childhood have been associated with
significant growth retardation or stunting (
Checkley et al., 2008
). Moreover,
malnutrition appears to place children at substantially increased risk for devel-
opment of diarrhea caused by ETEC. In addition, children with diarrheal illness
due to ETEC tend to have more severe diarrheal illness when they are malnour-
ished (
Black et al., 1984
;
Mondal et al., 2012
).
A small percentage of patients with traveler's diarrhea will experience more
chronic symptoms lasting months to years. The pathogenesis of these presum-
ably post-infectious sequelae, referred to as post-infectious irritable bowel
syndrome, is uncertain. Nevertheless characteristic low-grade inflammatory
changes in the mucosa could suggest ongoing untoward response to the prior
infection (
Connor, 2005
).
Diagnosis
Identification of ETEC in clinical specimens relies on the identification of heat-
labile and/or heat-stable toxins in fecal isolates of
E. coli.
While a number of
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