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( Bain and Green, 1999 ; Chaudhury et al., 1999 ), but the evidence for this sup-
position is weak. Genes associated with extraintestinal disease (e.g. papG ,
sfa/focG , cnf1 , ibeA , fyuA , iroN , and ompT ) are lacking in E. fergusonii , as are
intestinal disease factors such as astA , sat , pic , stx1, and eaeA . By comparison,
E. albertii is a known diarrheal pathogen of humans ( Huys et al., 2003 ; Oaks
et al., 2010 ; Ooka et al., 2012 ), an avian pathogen responsible for epidemic mor-
tality in finches in Alaska and Scotland ( Foster et al., 1998 ; Oaks et al., 2010 ),
and has been implicated in the death of other bird species ( Oaks et al., 2010 ). All
strains of E. albertii appear to possess the intimin locus and produce cyto-lethal
distending toxin B ( Oaks et al., 2010 ). Escherichia strains belonging to the cryp-
tic lineages CI-CV encode a variety of extraintestinal and intestinal virulence
factors, sometimes at high frequencies ( Ingle et al., 2011 ). However, with the
exception of clade I strains, there appears to be little evidence to suggest that they
are potential pathogens. Enterotoxigenic E. coli (ETEC) appear to have evolved
on multiple occasions and Steinsland et al. (2010) identified one clonal group of
ETEC strains, CG12, that they estimated to be atleast ten times older than all other
ETEC clonal groups. ETEC CG12 strains are members of cryptic clade I sug-
gesting that at least some members of this clade are potential diarrheal pathogens.
WHERE DOES E. COLI OCCUR?
E. coli can be isolated from plants and a wide variety of animals. While E. coli
can be recovered from ectothermic vertebrates it is more frequently encountered
in homeotherms ( Gordon and Cowling, 2003 ). However, even among birds and
mammals, factors such as body size and gut morphology are important predic-
tors of the likelihood of isolating E. coli from a particular host ( Gordon and
Cowling, 2003 ). In birds and carnivorous mammals the probability of detecting
E. coli in a host increases with the body size of the host. This outcome is likely
a consequence of the relationship that exists between body mass and gut transit
times. For example, in the carnivorous marsupials (Dasyuridae) gut transit times
vary from about 1 hour for the 18-g Sminthopsis crassicaudata to 13 hours for
the 1000-g Dasyurus viverrinus . Gut morphology also appears to play a role.
Insectivorous bats have relatively short undifferentiated tube-like intestines that
lack a cecum, while a similar-sized rodent has a well-differentiated intestine and
possesses a cecum. E. coli is much less frequently isolated from bats than from
similar-sized rodents. Experiments with rats fed diets differing in the concentra-
tion of crude fiber resulted, as expected, in food transit times through the gut
declining with increasing fiber concentration ( O'Brien and Gordon, 2011 ). These
experiments also demonstrated that E. coli cell densities declined with decreasing
transit times. Extrapolating the observed linear relationship between cell density
and gut transit time predicts that E. coli should not be found in animals such as
bats ( O'Brien and Gordon, 2011 ). A variety of other factors may also influence
E. coli cell densities in a host. For example, pregnancy coupled with excessive
weight gain ( Santacruz et al., 2010 ) or starvation in children ( Monira et al., 2011 )
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