Biology Reference
In-Depth Information
As a first approximation it may be stated that every human harbors a differ-
ent numerically dominant strain of E. coli . In a study of fecal isolates recovered
from 228 people, it was found that only 27% of the observed clones were recov-
ered from more than one individual ( Johnson et al., 2008 ). However, the sharing
that did occur was highly structured. Strain sharing was observed in 313 of the
total potential sharing pairs, however 27% of within-household pairs shared a
clone, while only 0.8% of across-household pairs did.
HOST SPECIFICITY
Does E. coli exhibit host-specificity? It depends who you ask. Part of the problem
relates to definition. Do we confine host specificity to situations where there is a
one-to-one match between host species and partner organism? Or do we think of
it in terms of host preference, where the probability of detecting the partner var-
ies among different host species. At the species level there is clear evidence that
E. coli is most likely to be isolated from warm-blooded vertebrates that have either
a cecum or a body mass greater than a kilogram ( Gordon and Cowling, 2003 ).
Although there is some evidence to suggest that strains of the various phylo-
groups exhibit some degree of host preference ( Figure 1.2 ), it is also clear that other
factors can influence phylo-group membership of E. coli isolated from a single
host species, such as humans ( Figure 1.3 ). Until recently there has been little evi-
dence to indicate that the vast majority of commensal isolates of E. coli exhibit host
specificity. However, it has been suggested that there are animal-specific strains
( Escobar-Páramo et al., 2006 ), as well as human-specific strains ( Clermont et al.,
2008 ). Some clonal groups, ST 95 and ST 69, for example, are frequently isolated
from the feces of asymptomatic humans living in Australia, yet neither of these STs
has ever been detected in a native Australian mammal (unpublished data).
Among researchers primarily concerned with E. coli that causes extraintes-
tinal infection, many believe that hosts such as poultry and companion animals
can serve as reservoirs for strains responsible for human infections. Indeed, near
identical strains can be isolated from human and animal feces ( Reeves et al.,
2011 ). Among researchers focused on the intestinal pathogens, host specific-
ity is virtually dogma. Whereby, most of the various pathotypes (EPEC, EIEC,
ETEC, DAEC, EAEC) are host specific, with the exception of classic human
EHEC strains that have a ruminant reservoir. For the non-EHEC pathotypes, the
available evidence does indicate that the great majority of strains capable of caus-
ing disease are indeed host specific ( Nataro and Kaper, 1998 ; Robins-Browne
and Hartland, 2002 ; Bardiau et al., 2010 ; Croxen and Finlay, 2010 ).
POPULATION DYNAMICS OF INTESTINAL PATHOGENS
The population dynamics of many of the intestinal E. coli pathogens of humans
and domesticated animals have many similarities to classic infectious dis-
eases such as measles ( Hartley et al., 2005 ). For a pathogen to persist in a host
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