Biology Reference
In-Depth Information
SOR fermentation and GUD activities, resulting in the present day GUD
-
SOR
-
strain containing Stx1, Stx2, and the EHEC plasmid (
Reid et al., 2000
;
Wick et al.,
2005
).
E. coli
O157:H7 is believed to be continuously evolving by mutating exist-
ing genes and by acquiring novel virulence factors, mostly by means of gene
transfer through bacteriophage transduction. Several T3SS effectors in EHEC
are phage-encoded, and recent studies have found that phage-encoded regu-
lators also influence the expression of virulence factors such as T3SS (
Tree
et al., 2011
;
Flockhart et al., 2012
). Advances in sequencing and molecular
typing methods, such as multi-locus sequence typing, have made feasible the
documentation of the ongoing evolution of this organism. Using whole genome
sequencing and single nucleotide polymorphism (SNP) analysis of clinical iso-
lates of STEC O157, several recent studies suggest the emergence of a highly
virulent clade of STEC O157 that has gained new virulence genes (
Manning
et al., 2008
). Strains belonging to this new clade (clade 8) were responsible for
recent outbreaks in the US associated with leafy vegetables, all of which led to
high rates of hospitalization and HUS. Clade 8 strains were also implicated in a
recent outbreak in Japan (
Yokoyama et al., 2011
).
Thus, the ability of
E. coli
strains to acquire virulence factors through hori-
zontal gene transfer continues to generate novel and unusual STEC pathotypes
with increased pathogenicity. A clear example is the highly virulent Shiga toxin-
producing enteroaggregative
E. coli
O104:H4, the causative agent of the recent
German STEC outbreak (see Chapter 11). This strain is believed to have emerged
as a result of transduction of enteroaggregative
E. coli
(EAEC) with Stx phage
(
Rasko et al., 2011
). This hybrid strain therefore apparently has the capacity to
effectively colonize the human gastrointestinal tract and the ability to produce Stx,
making it exceptionally virulent. It is clear that the continuous evolution of STEC
can produce new public health threats. A thorough understanding of the extent to
which the genomic plasticity of STEC contributes to its pathogenicity and evolu-
tion is necessary for our ability to rapidly respond to emerging and potentially
deadly STEC strains. For more details on
E. coli
evolution, see Chapter 3.
Epidemiology and global impact
STEC infection is a notifiable disease in the US and several other countries
(
Chang et al., 2009
). It is highly prevalent in the US, countries of the European
continent, the UK, Japan, Argentina, and Australia, although the predominant
serotype varies with location (
Table 5.1
). In the US, following the first out-
break in 1982, the number and severity of STEC outbreaks has dramatically
increased. According to the CDC (
Centers for Disease Control and Preven-
tion, 2012
), STEC causes approximately 265,000 cases of illness, including
3,600 hospitalizations, and 30 deaths in the US each year (
Scallan et al., 2011
).
E. coli
O157:H7 is the predominant STEC serotype responsible for human
disease in the US (
Tarr et al., 2005
), causing more than 96,000 cases of illness
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