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heavy metals (e.g. cadmium, mercury, silver), and other survival factors against
lethal doses of antimicrobials (
Mayer et al., 1995
;
Bennett, 2008
;
Hawkey, 2008
).
In addition, plasmid genes up-regulate important virulence and fitness genes in
chromosomes through extensive cross-talk between plasmid and chromosome,
as evidenced in many enteropathogenic
E. coli
(EPEC) strains (
Schmidt, 2010
).
For example, the products of
per
genes in EPEC plasmids regulate expression
of the pathogenicity locus of enterocyte effacement (LEE) genes (
Mellies et al.,
1999
). Complex synergistic activities accelerate plasmid spread. For example,
dense, structured populations as in biofilms increase the possibility of plasmid
transfer by conjugation (see below) (
Reisner et al., 2006
). By the same token, the
conjugation apparatus and the release of DNA stimulate formation and mainte-
nance of biofilms (
Molin and Tolker-Nielsen, 2003
). Other examples of plasmid-
borne virulence factors include Bundle-forming pili of EPEC (
Donnenberg et al.,
1992
); EhxA in EHEC (
Burland et al., 1998
); pCoo in ETEC (
Froehlich et al.,
2005
); plasmid-encoded toxin (Pet) in EAEC (
Eslava et al., 1998
); IcsA (VirG) in
EIEC/
Shigella
(
Buchrieser et al., 2000
); TraT in UPEC (
Timmis et al., 1985
), etc.
Prophages
Temperate phages upon DNA injection into the host bacteria do not immediately
enter into the lytic cycle but can instead integrate into the bacterial genome as a
prophage. In fact, most of the mosaic gene elements in the
E. coli
genome are
of a prophage nature (
Canchaya et al., 2003
). Most prophage genes are usually
silent during bacterial growth and reproduction and are functional only when the
prophage is activated (induced), i.e. enters the lytic pathway to produce active
phages and lyse the host cell (usually under stress conditions, like UV light,
antibiotic exposure, etc.), e.g. Shiga toxins Stx1 and Stx2 of EHEC (
Dobrindt,
2005
). However, some prophages commonly carry genes that are expressed and
can add new phenotypic traits to their hosts that are important for success in colo-
nization and competition within the habitat (
Brussow et al., 2004
). In EHEC and
EPEC genomes, for example, a diversity of the prophages encode characteristic
virulence factors (
Ohnishi et al., 2002
). A few examples are several type III secre-
tion system (T3SS) effector proteins of EHEC and EPEC such as Cif (
Marches
et al., 2003
), EspF
U
(
Campellone et al., 2004
), EspJ (
Dahan et al., 2005
), EspK
(
Vlisidou et al., 2006
), NleA (
Gruenheid et al., 2004
), TccP (
Garmendia et al.,
2004
) (see Chapters 4, 5, and 15). Other examples include cytolethal distending
toxins in EPEC (
Asakura et al., 2007
); type II heat-labile enterotoxin in ETEC
(
Jobling and Holmes, 2012
); GtrAB in EIEC/
Shigella
(
Chaudhuri et al., 2010
).
Interestingly, until recently, there were no known major virulence determinants
encoded by prophages in UPEC (
Lavigne and Blanc-Potard, 2008
).
Chromosomal islands
Chromosomal islands characterize a highly diverse group of DNA elements,
with a broad range in size and abundance across the bacterial chromosomes
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