Enteroaggregative Escherichia coli - Escherichia coli: Pathotypes and Principles of Pathogenesis - page 240

been described ( Itoh et al., 1997 ). Risk factors for EAEC infection include
travel to developing countries, ingestion of contaminated food and water, poor
hygiene, host susceptibility, and possibly immunosuppression ( Nataro et al.,
1985 ; Okeke and Nataro, 2001 ; Huang and Dupont, 2004 , 2006 ).
Definitive data demonstrating pathogenicity of individual EAEC strains is
sparse. In volunteer studies, archetype strain 042 elicited clinical diarrhea in
three of five subjects, and enteric symptoms in another ( Nataro et al., 1995 ). In
a prior study, strain JM221 elicited enteric symptoms in some patients. Interest-
ingly, however, some other EAEC strains failed to cause diarrhea in volunteers.
These results suggest heterogeneity of EAEC virulence, although the molecu-
lar basis of this variation remains elusive. Some studies suggest that children
are more likely to be affected in the first month of life ( Gonzalez et al., 1997 ;
Gascon et al., 1998 ), while others have stressed that most cases arise in older
children ( Okeke et al., 2000a ). These disparate epidemiologic observations
could be reconciled by diverse virulence characteristics of the strains circulat-
ing at the respective sites, in combination with a variety of host immunity and
host resistance.
Outbreaks
The first reported EAEC outbreak occurred in a Serbian nursery in 1995
( Cobeljic et al., 1996 ); of the 19 afflicted infants, three developed persistent
diarrhea. There have been two EAEC outbreaks reported in Mexico City ( Eslava
et al., 1993 ). Itoh et al. (1997) described a massive outbreak of EAEC diarrhea
among Japanese children, affecting nearly 2700 patients. Outbreaks have also
been reported among adults in the UK ( Smith et al., 1997 ).
Morabito et al. (1998) described an outbreak of hemolytic uremic syndrome
(HUS) in France caused by a Shiga toxin-producing EAEC strain. Sporadic
small outbreaks of hemolytic uremic syndrome (HUS) have been attributed to
Stx-producing EAEC of the O111:H2, O111:H21, and O104:H4 serotypes over
the last 15 years ( Morabito et al., 1998 ; Frank et al., 2011 ; Scheutz et al., 2011 );
however, they were localized to small populations in France, Ireland, and the
Republic of Georgia and were not disseminated throughout Europe.
From May through June 2011, Europe was struck by an outbreak of massive
proportions, infecting 4137 individuals and resulting in 54 deaths (see Chapter
11). By epidemiological linking, contaminated sprouts were found to be the
source of the outbreak, although not isolated from the source ( Frank et al.,
2011 ; Scheutz et al., 2011 ). There are troubling differences between the Ger-
man outbreak and previous large outbreaks: (i) HUS represented 22% (845) of
the ascertained cases, which is a much higher proportion than in other outbreaks
(6-10%); (ii) it was predominately seen in healthy adults, which was highly
uncommon with diarrhea-associated HUS, that occurs primarily in children;
and (iii) the causative agent was a non-O157 Stx-producing EAEC strain of
serotype O104:H4 ( Frank et al., 2011 ).