Enteroaggregative Escherichia coli - Escherichia coli: Pathotypes and Principles of Pathogenesis - page 254

1997 ; Olesen et al., 2005 ; Boisen et al., 2012 ). Moreover, a high frequency of
EAEC strains expresses untypable O antigens and H antigens or are non-motile
( Nataro and Kaper, 1998 ; Uber et al., 2006 ; Regua-Mangia et al., 2009 ). Never-
theless, there exist commonly isolated EAEC serotypes (O44:H18, O111:H12,
O125, and O126 strains). Studies show that some serotypes of the traditional
enteropathogenic E. coli such as O55, O111, O86, O126, and O128 can be found
in EAEC ( Nataro et al., 1998 ; Suzart et al., 1999 ; Elias et al., 2002 ) although the
most commonly found serogroups reported in EAEC are O86, O126, and O125
( Spencer et al., 1999 ; Sarantuya et al., 2004 ; Uber et al., 2006 ). It was suggested
that the occurrence of EPEC O serogroups (O126, O128, and O158) along with
EAEC markers influenced the positive association of E. coli strain with diarrhea
( Pereira et al., 2007 ). Serotyping is often useful in the characterization of other
pathogenic E. coli , however it is of little value in EAEC diagnostics ( Okeke and
Nataro, 2001 ). However, in a detailed study on genomic characterization by
Boisen et al. (2012) , targeting a collection of 121 EAEC strains isolated from
children in Mali with or without moderate to severe diarrhea, it was found that
strains expressing the H33 flagellar antigen were found significantly more often
in cases than in controls. This association may signify the existence of a specific
set of virulence genes in strains of this H type ( Boisen et al., 2012 ). A phyloge-
netic framework was presented identifying three major clusters of DEC contain-
ing EAEC. Members of each group show conserved plasmids and chromosomal
loci, which indicates that most EAEC, like EPEC, feature conserved linkage
of virulence genes ( Czeczulin et al., 1999 ). EAEC strains that did not fall into
the above-mentioned clusters could be milder pathogens eliciting inflammation
without diarrhea ( Steiner et al., 1998 ). Notably, the pAA plasmid of EAEC is,
however, heterogeneous with regard to fimbria and toxin expression. In volun-
teer studies, three strains expressing the AAF/I variant did not induce diarrhea,
whereas the one strain expressing AAF/II caused diarrhea in the majority of
infected subjects ( Nataro et al., 1995 ).
IDENTIFICATION OF EAEC
The gold standard for identifying EAEC is the HEp2-cell adherence assay
( Nataro and Kaper, 1998 ) in as much as the pathogen was initially defined by
the presence of a characteristic stacked brick pattern, designated aggregative
adherence (AA) in this assay ( Nataro et al., 1987 ). The HEp2-cell adherence
assay is unfortunately not designed to screen large numbers of colonies from
stool samples as it is very time consuming and is further limited by the risk of
contamination of the cell cultures. A DNA probe, CVD432 from the pAA plas-
mid of EAEC, has been reported to be specific for EAEC but varies in sensi-
tivity ( Baudry et al., 1990 ). As reviewed, the sensitivity variation was between
20% to 89% when compared to the HEp2-cell adherence assay ( Okeke, 2009 ).
The CVD432 probe has been shown to correspond to the aatA gene, which
encodes a transporter for the dispersin protein (Aap), also regulated by AggR