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Infection and Immunity, February 1999, p. 546-553, Vol. 67, No. 2
Laboratoire de Microbiologie,
Received 27 April 1998/Returned for modification 13 July
1998/Accepted 5 November 1998
Previous studies suggesting a link between Escherichia
coli phylogenetic groups and extraintestinal virulence have been
hampered by the difficulty in establishing the intrinsic virulence of a bacterial strain. Indeed, unidentified virulence factors do exist, and
the susceptibility of the host to infection is highly variable. To
overcome these difficulties, we have developed a mouse model of
extraintestinal virulence to test the virulence of the strains under
normalized conditions. We then assessed the phylogenetic relationships
compared to the E. coli reference (ECOR) collection, the
presence of several known virulence determinants, and the lethality to
mice of 82 human adult E. coli strains isolated from normal
feces and during the course of extraintestinal infections. Commensal
strains belong mainly to phylogenetic groups A and B1, are devoid of
virulence determinants, and do not kill the mice. Strains exhibiting
the same characteristics as the commensal strains can be isolated under
pathogenic conditions, thus indicating the role of host-dependent
factors, such as susceptibility linked to underlying disease, in the
development of infection. Some strains of phylogenetic groups A, B1,
and D are able to kill the mice, their virulence being most often
correlated with the presence of virulence determinants. Lastly, strains
of the B2 phylogenetic group represent a divergent lineage of highly
virulent strains which kill the mice at high frequency and possess the
highest level of virulence determinants. The observed link between
virulence and phylogeny could correspond to the necessity of virulence
determinants in a genetic background that is adequate for the emergence
of a virulent clone, an expression of the interdependency of
pathogenicity and metabolic activities in pathogenic bacteria.
In humans, strains of the species
Escherichia coli can be commensal (since they are part of
the normal intestinal microbial flora) and/or the cause of various
infectious diseases (intestinal and extraintestinal infections)
(2, 10). The barrier between commensalism and virulence
results from a complex balance between the status of the host and the
presence and expression of virulence factors in the bacteria. The
genetic structure of E. coli can be considered clonal
(37), and, indeed, various intestinal (41) or
extraintestinal (1, 26, 38) E. coli infections
have been linked to specific clones or groups of related clones. In several cases, pathogenicity has been correlated with the presence of
genes encoding virulence factors organized on large blocks, called
pathogenicity islands. It has been shown, further, that pathogenicity
islands can disseminate horizontally between distinct E. coli strains whether they are located on plasmids, bacteriophages, or even the bacterial chromosome (16). Horizontal transfer
in E. coli has also been reported for other systems,
including the O antigen, the hsd restriction-modification
system, and some housekeeping genes (28). It has been shown,
however, that horizontal transfer, in general, does not disrupt the
clonal structure of the species (9, 15, 27, 28). An
attractive hypothesis to reconcile horizontal dissemination of
virulence factors and oligoclonality of the virulent strains would be
that of an interaction between virulence determinants and the genetic
background of the bacteria. Recent attempts at establishing the
phylogenetic position of virulent clones within the diversity of the
species as a whole seem to support this hypothesis (5, 36).
However, the conclusions derived from these studies are weakened by the
difficulty in appreciating the intrinsic virulence of a given bacterial
strain. Indeed, the direct search for virulence determinants is
obviously limited to the known determinants, and unidentified virulence
factors do exist. Second, it has been shown that the status of the host can be critical to the development of an infection, independent of the
presence or absence of virulence factors and/or of chromosomal genetic
markers (5, 20, 25, 33, 40). Finally, various other
environmental parameters such as the amount of the inoculum can
influence the course of an infection. Thus, the "virulent" or
"nonvirulent" character of a strain cannot be systematically inferred from the circumstances in which the strain was isolated (commensal or pathogenic).
To clarify this issue, we have developed a mouse model to evaluate the
intrinsic extraintestinal virulence of bacterial strains in normalized
conditions. Using this model, we have determined the lethality to mice
of a series of 82 human E. coli strains isolated from normal
feces and during the course of extraintestinal infections. These
strains were further characterized by studying the distribution of
known virulence factors and their phylogenetic relationships with
respect to the E. coli reference (ECOR) collection (30). Our data, taken together, establish the link between
phylogeny and extraintestinal virulence in the E. coli species.
Bacterial strains.
A total of 82 E. coli strains
isolated from adult humans were studied that belonged to a previously
published collection of 85 commensal isolates and 191 extraintestinal
pathogenic isolates (isolated from patients with urinary tract
infections, septicemia, and miscellaneous infections including
cholecystitis, ascites, and lung infections) (12, 13). A
study of the carboxylesterase B polymorphism distinguished two
electrophoretic types among these strains: B1
(MF Animal model.
Pathogen-free female of the outbred white
Swiss mice lineage (Rj: Swiss-IOPS Orl) (6 to 8 weeks old, 25 to
30 g) were purchased from the Centre d'Elevage R. Janvier (Le
Genest, Saint Isle, France). E. coli strains were stored in
glycerol solution at rrn restriction fragment length polymorphism (RFLP)
analysis (ribotyping).
Total E. coli DNA was prepared
as previously described (3). It was digested with
EcoRI and HindIII and subjected to Southern blotting analysis with ribosomal 16S+23S RNA from E. coli as
a probe. The probe was labeled by random oligopriming with a mixture of
hexanucleotides (Pharmacia, Uppasala, Sweden) and cloned Moloney murine
leukemia virus reverse transcriptase (Bethesda Research Laboratories,
Inc., Gaithersburg, Md.) in the presence of 0.35 mM DIG-11-dUTP
(digoxigenin-11-deoxyuridine-5' triphosphate; Boehringer, Mannheim,
Germany). The procedure for chemiluminescence detection was as already
reported (4).
Detection of virulence determinants.
The virulence
determinants surveyed in this work for the 82 E. coli
strains were chosen as they were relevant to extraintestinal infections
(29). The capsular type K1 common among pathogenic E. coli strains was detected phenotypically with an antiserum to
Neisseria meningitidis group B (8).
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
The Link between Phylogeny and Virulence in
Escherichia coli Extraintestinal Infection
Hôpitaux de
Paris,2
INSERM U
4583 and
Laboratoire de Recherche en
Bactériologie Pédiatrique (JE 2255),
ABSTRACT
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Abstract
Introduction
Materials and methods
Results
Discussion
References
INTRODUCTION
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Abstract
Introduction
Materials and methods
Results
Discussion
References
MATERIALS AND METHODS
Top
Abstract
Introduction
Materials and methods
Results
Discussion
References
68 to 72) and B2
(MF 57 to 63). Strains of carboxylesterase B
type B2 were more frequently pathogenic and often produced
alpha-hemolysin and mannose-resistant hemagglutinin (MRHA) whereas
strains of type B1 were prevalent in commensal isolates and
devoid of these virulent factors. The 82 E. coli strains
used in this study were selected for their commensal (12) or
pathogenic (13) origin, their carboxylesterase B
electrophoretic types B1 and B2
(13), and their production of 
-hemolysin and MRHA. Six
groups were constituted according to these criteria: group 1 (15 strains), commensal, carboxylesterase B1 type,
nonhemolytic, MRHA negative; group 2 (18 strains), pathogen,
carboxylesterase B1 type, nonhemolytic, MRHA negative;
group 3 (12 strains), pathogen, carboxylesterase B1 type,
nonhemolytic, MRHA positive; group 4 (10 strains), pathogen,
carboxylesterase B2 type, nonhemolytic, MRHA negative;
group 5 (15 strains), pathogen, carboxylesterase B2 type,
nonhemolytic, MRHA positive; group 6 (12 strains), pathogen, carboxylesterase B2 type, hemolytic, MRHA positive (Table
1).
TABLE 1.
Characteristics of the 82 E. coli
clinical strainsa
70°C. The strains were isolated in Trypticase
soy agar (AES Laboratories, Combourg, France) and then grown in
Trypticase soy broth medium (pH 7.3, osmolarity = 271 mOsm/l) (AES
Laboratories) and incubated with shaking at 37°C to a density of
109 bacteria per ml (approximately 4 h). The bacterial
count was determined by measuring the optical density at 530 nm. A 2-ml sample of the culture was then centrifuged at 2,500 × g for 10 min, washed twice with Ringer solution, and
resuspended in Ringer solution. These suspensions were used to
inoculate the mice subcutaneously in the abdomen or intraperitoneally.
Ten mice were inoculated with each strain. After inoculation, the mice
were observed every hour for the first 6 h, at 18 h and daily
for up to 1 week. Death and its delay were noted for each mouse. Dead
animals were dissected, and the liver, spleen, and kidneys were
inspected macroscopically and sampled. Each organ was washed with
Ringer solution, weighed, and crushed with 5 ml (spleen and kidneys) or
10 ml (liver) of sterile Fontainebleau sand. Successive dilutions of
the crushed organs were obtained (from 10
1 to
107) with Ringer solution and inoculated on Trypticase
soy plates. One drop of heart blood was also inoculated on the same
medium. The plates were incubated at 37°C for 24 h, and the
colonies were counted.
Statistical analysis.
The 82 clinical strains were compared
to the 72 strains of the ECOR collection by a statistical treatment of
the rrn RFLP data to assign these strains to the
phylogenetic groups A, B1, B2, and D previously delineated among the
ECOR strains (17). The rrn RFLP data were
summarized as two-way tables of 72 rows for the 72 ECOR strains
(9) and of 82 rows for the 82 E. coli clinical
strains, with the number of columns corresponding to the number of
rrn-containing DNA fragments detected by
HindIII and EcoRI endonucleases. For each
column, the rrn-containing fragment was coded as a binary
code, present = 1 or absent = 0, according to the strains. A
factorial analysis of correspondence (FAC) (14, 21, 39) was
first conducted on the ECOR strain data. FAC is an eigenvector method
of ordination similar to a principal-component analysis. However, it
differs from the latter by the use of a covariance matrix based on
2 distances rather than a covariance matrix based on
Euclidean distances. Both techniques describe the dispersion and shape
of a cloud of n objects (here, the ECOR strains) or
p variables (here, p was the number of
rrn containing DNA fragments detected by
HindIII and EcoRI) in a multidimensional
space, by replacing the original data set by a new set of orthogonal
linear coordinates in a space of significantly lower dimension. The
explained variances of the elements of the data set (the strains and
the rrn DNA fragments) are in decreasing order of magnitude
with respect to these new coordinates. Furthermore, the variables used
for FAC are categories, whereas those used for principal-component
analysis are quantitative or continuous variables. The computation
determines a plane defined by the first two principal axes of the
analysis; the first axis, F1, accounts for most of the variance, and
the second axis F2, orthogonal to F1, accounts for the largest part of
the variance that is not accounted for by F1. Each of the 72 ECOR
strains is thus projected on the plane F1/F2, and their respective
projections on this plane allows the subclassification of E. coli into four main phylogenetic groups. In a second step, the 82 clinical strain data were considered to be supplementary observations
and projected on the principal plane F1/F2 obtained with the ECOR
strains. Their projections in the different areas corresponding to each
phylogenetic group allows their classification into these groups.
2 test.
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RESULTS |
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Abstract
Introduction
Materials and methods
Results
Discussion
References
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Lethality in mice. To obtain reproducible results and a clear-cut interpretation of the data, it was important first to standardize the model. To do so, the size of the inoculum from 103 to 109 CFU was tested for one strain of group 1 with no virulence determinants (strain 1) and for one strain of group 6 with numerous virulent determinants (strain 71). For these two strains, two routes of inoculation (subcutaneous and intraperitoneal) were assayed. The mice were observed continuously during the first 6 h following inoculation to detect whether rapid death was linked to endotoxinic shock. From these preliminary steps, we retained the less invasive subcutaneous route of inoculation with 108 CFU in 0.2 ml of Ringer solution. Under these conditions, no mouse died within the first 6 h and the animals could be clearly classified as "killed" from infection or "survivors." Bacterial counts in the liver, spleen, and kidneys of the killed mice were greater than or equal to 108 CFU per ml. Animals surviving for more than 7 days were considered permanent survivors, since tissue and blood cultures from these mice, sacrificed on this date after the inoculation, were sterile.
Of the 82 E. coli strains we studied, 38 killed at least one mouse (Table 1). Of these 38 strains, 32 (84.2%) killed 9 or all 10 of the 10 inoculated mice. Thus, "lethality" is a rather clear-cut parameter since when it is noted for a given strain, it is so most of the time for all or almost the inoculated mice. In addition, of the 32 strains which killed 9 or 10 mice, 27 (84.4%) did so in a short period, since more than 6 of the 10 mice inoculated with each strain died in less than 18 h. A clear difference in lethality was observed among the six groups of strains. For the strains of groups 1 and 2, no strains, except one (group 2), killed the mice. Thus, a discrepancy is observed between the pathogenic origin of the strains of group 2 and their lack of virulence in the animal model. In contrast, all the strains of groups 5 and 6, except one, did kill the mice. Strains of groups 3 and 4 exhibited an intermediate behavior, with approximately 50% of them killing the mice. Considering only the strains which were lethal for the mice, no significant difference was observed between the groups in terms of the number of mice killed by a given strain or the rapidity with which the strains killed the mice.Phylogenetic distribution of the E. coli strains. To assess the phylogenetic relationships among strains, statistical analysis by FAC was performed with the rrn RFLP data obtained for the clinical and ECOR (9) strains. The results are expressed as the projections of each strain on a plane defined by two axes (F1 and F2) which account for most of the total variance (Fig. 1). As previously described (5, 9), this analysis divides the ECOR strains into four main phylogenetic groups (A, B1, B2, and D) and these groups correspond to the classification initially reported by Hertzer et al. (17) from their analysis of 38 metabolic enzymes.
|
), 2 (
), 3 (
), 4 (
), 5 (
), and 6 (
),
considered supplementary observations, are projected in the F1/F2
plane. This plane, obtained by computation, is defined by the two
principal axes of the analysis; the first axis, F1, explains most of
the variance, and the second axis, F2 (orthogonal to F1), explains most
of the variance which is not explained by F1. Phylogenetic groups A,
B1, B2, and D ( 72 and
MF 68 electrophoretic variants of
carboxylesterase B (13). As expected from previous studies
(34, 35), pathogenic strains of the three remaining groups,
4, 5, and 6, which all belonged to the carboxylesterase B type
B2, were classified in phylogenetic group B2.
Detection of virulence determinants.
Overall, a progressive
enrichment of virulence determinants was observed, from the strains of
groups 1 and 2, which lack virulence factors, to the strains of group
6, which possess the highest level of virulence determinants. The K1
antigen was detected in 15 isolates. Of these, 13 belong to
phylogenetic group B2. There was a good phenotype-genotype correlation
for the adhesin and hemolysin determinants. The rare discrepancies
observed between phenotype and genotype were not judged significant,
since previous reports indicate variable in vitro phenotypes of
virulence factors due to the in vitro culture conditions (11, 25,
31). The afa operon was rarely detected (three strains
in group 3). The pap operon was found in strains of
phylogenetic groups D, B1, and B2 but was significantly more frequent
in the B2 group (2 = 25.27; P < 0.0005), whereas the sfa/foc operon is strictly restricted to strains of the B2 phylogenetic group. Thus, the strains
of the B2 phylogenetic group more often possess an adhesin-encoding operon than do strains of the other phylogenetic groups, whatever the
level of MRHA expression. As expected, the ibe10 gene, which is involved in the pathogenesis of meningitis in newborns
(18), was rarely found (five strains) and was strictly
restricted to strains belonging to the B2 phylogenetic group. The
hly determinant was significantly more frequent in strains
of phylogenetic group B2 (2 = 12.29; P < 0.005). The aer determinant was widespread in strains of
all the phylogenetic groups. This can be explained by the fact that we
did not differentiate the episomal from the chromosomal aer
operon. It has been shown that carboxylesterase B type B1 strains carry a plasmid-encoded aerobactin system whereas
carboxylesterase B type B2 strains carry chromosomal
aerobactin determinants (19). The eaeA
determinant was not detected in any of the 82 studied clinical strains.
Whole-data analysis. A FAC analysis was conducted on the whole data, taking as variables the origin of the strains, carboxylesterase B type, phylogenetic group, virulence determinants, and lethality to mice. When the distribution of these variables was studied, the first two principal axes, F1 and F2, accounted for 47.41% of the total variance and projections of the variables on the F1/F2 plane showed very striking features (Fig. 2A). Indeed, the F1 axis, which accounted for 37.25% of the total variance, clearly showed two opposite classes of determinants. Its negative values were lethality to mice, phylogenetic group B2, carboxylesterase B type B2, detection of sfa/foc, hly, and pap operons and of the ibe10 gene, detection of K1 antigen, and, to a lesser degree, detection of aer and pathogenic origin. Its positive values were commensal origin, absence of lethality to mice, carboxylesterase B type B1, and phylogenetic groups B1 and A. Phylogenetic group D and the afa detection were clearly singled out from their highly negative values on the F2 axis.
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DISCUSSION |
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Abstract
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Materials and methods
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Discussion
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To our knowledge, this is the first report to provide an overview of extraintestinal virulence in E. coli by combining data on commensal and pathogenic strains tested for global virulence in a standardized mouse model, for the presence or absence of several known virulence determinants, and for their classification into the different phylogenetic groups of the E. coli species. Our mouse model is able to account for a large potential of virulence and is not hampered by the variability of the susceptibility to infection of the host.
From the whole-data analysis (Fig. 2A), we clearly show that there is a link between phylogenetic group, detection of virulence determinants, and lethality in mice. Carboxylesterase B type B2 strains, which correspond to B2 phylogenetic group strains (34, 35), are rare in the feces in commensal situations. They represent 7% (in Western countries) to 3% (in developing countries) of the commensal E. coli population (12). Similarly, phylogenetic group D strains are underrepresented in the human commensal strains; in our series, the commensal strains, which all belong to carboxylesterase B type B1 (group 1), are exclusively composed in equal proportion of strains of phylogenetic groups A and B1, devoid of pathogenic determinants and not lethal for the mouse. The pathogenic strains of group 2 exhibit exactly the same characteristics as the commensal strains since all but one of them do not kill the mice, they are devoid of the tested virulence genes, and they belong to the phylogenetic groups A and B1 (Table 1). Indeed, if the "pathogenic" and "commensal" parameters are not taken into account for the whole-data analysis, the two clearly separated clusters of 7 and 12 strains for the A phylogenetic group and of 8 and 12 strains for the B1 phylogenetic group in Fig. 2B, respectively, merge into a single cluster for the A group and a single cluster for the B1 group (data not shown) without affecting the position of the rare virulent strains in these two groups (strains 44, 18, 36, and 39). This suggests that the pathogenic origin of the strains of group 2 could be related to various host-dependent factors, such as susceptibility linked to an underlying disease or site whereby the organisms gain entry. This is in agreement with the previous epidemiological studies, which have shown that strains with no virulence determinants can infect a host that has been made susceptible (5, 20, 25, 33, 40). This also explains that the character "pathogenic origin" (pat+) in Fig. 2A is at an intermediate position on the first axis as opposed to the parameter "lethality." Still, strains of all phylogenetic groups are able to be lethal for mice. Even though phylogenetic D group strains are clearly underrepresented in our panel, it is clear that strains of this phylogenetic group as well as strains of the B1 phylogenetic group can be highly virulent for the mice, since they killed more than six mice in less than 18 h, in agreement with the presence of virulence determinants. Lastly, B2 phylogenetic group strains are clearly the most virulent strains for the mice, again in agreement with the presence of virulence determinants. Their wide distribution in the B2 area of the F1/F2 plane of the FAC analysis (Fig. 1) illustrates that they are genetically heterogeneous in accordance with the carboxylesterase B2 polymorphism (Table 1). It should be noted that in the rrn RFLP FAC analysis (Fig. 1), a clear-cut distribution between phylogenetic groups A, B1, and D and phylogenetic group B2 is observed, reinforcing the deep genetic divergence of this particular group of strains among the E. coli species (23, 32).
Our set of adult extraintestinal E. coli strains can be linked to other extraintestinal E. coli strain collections, strengthening the prominent role of the B2 phylogenetic group strains in extraintestinal infection. The EcoRI rrn RFLP pattern presented in Fig. 2 of the paper by Maslow et al. (26) which describes 187 bloodstream E. coli isolates from patients in Boston and Nairobi, Kenya, can be compared to our data. Indeed, it is clear that their ribotypes A, B2, and E, which are found only in their cluster III containing 65% of the isolates (26), correspond to ribotypes that we have observed only within phylogenetic B2 group strains (Fig. 3 in the paper by Picard et al. [34] and data not shown). Furthermore, sfa-positive strains of Maslow et al. belong only to cluster III, and we have shown in this work and also previously (5) that sfa/foc operons are found only in the phylogenetic B2 group. Similarly, EcoRI rrn RFLPs and hly operon data presented by Arthur et al. (1), when studying uropathogenic isolates, allows the conclusion that their group IV, which encompasses the majority of the strains, corresponds to phylogenetic B2 group strains. According to the common O18:K1:H7 strains studied by Selander et al. (38) and Bingen et al. (5) and to the virulence determinant distribution, most of the neonatal meningitis strains of group 1 of Selander et al. correspond to phylogenetic B2 strains. This is in accordance with the data of Bingen et al., who found that 68% of the neonatal meningitis isolates belong to the B2 phylogenetic group (5). This high proportion of B2 phylogenetic group strains in human extraintestinal infections is not specific to humans and is also observed in nonhuman mammalian extraintestinal infections (7). Finally, although the ECOR collection is not representative of human isolates, the phylogenetic B2 group and, to a lesser extent, the phylogenetic D group strains have been shown to exhibit numerous virulence determinants compared to phylogenetic A and B1 strains (5, 6).
In conclusion, within the E. coli species, there is a phylogenetic group of strains, the B2 phylogenetic group, which is deeply divergent from the other strains and which represents the vast majority of strains involved in various extraintestinal infections. Such a distribution of virulence within phylogenetic groups in a species which remains clonal despite horizontal gene transfer (9, 15, 27, 28) allows the evolutionary hypothesis of an early genetic divergence within the E. coli species which led to phylogenetic group A and B1 commensal strains, on the one hand, and to the B2 phylogenetic group of pathogenic strains, on the other. This latter group of strains evolved toward extraintestinal virulence by acquisition of numerous pathogenic determinants (23). The observed stable link between virulence and phylogeny could correspond to the necessity of having virulence determinants into the right genetic background for the emergence of a virulent clone, an expression of the interdependence of microbial pathogenicity and metabolic activities in pathogenic bacteria (10). Selection could have favored strains of intermediate or high levels of virulence, since they compensate for the loss of transmission opportunities that result from killing or debilitating their hosts by increased fitness in the presence of host defenses or other bacterial strains (24).
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ACKNOWLEDGMENTS |
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We are grateful to Xavier Nassif for helpful discussions, to Juliette Chapron for her advice on statistical analysis, and to Francine Grimont for providing us with E. coli E2348/69.
This work was supported in part by the Programme Hospitalier de Recherche Clinique (grant AOM 96069).
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FOOTNOTES |
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* Corresponding author. Mailing address: INSERM U 458, Hôpital Robert Debré, 48 blvd. Sérurier, 75395 Paris cedex 19, France. Phone: 33 140 03 19 31. Fax: 33 1 40 03 22 77. E-mail: denamur{at}infobiogen.fr.
This paper is dedicated to the memory of Philippe Goullet, a
pioneer in the analysis of the genetic structure of E. coli.
Editor: R. N. Moore
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Abstract
Introduction
Materials and methods
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Discussion
References
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(2001). Commensal Escherichia coli isolates are phylogenetically distributed among geographically distinct human populations. Microbiology
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Gordon, D. M.
(2001). Geographical structure and host specificity in bacteria and the implications for tracing the source of coliform contamination. Microbiology
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Picard, B., Duriez, P., Gouriou, S., Matic, I., Denamur, E., Taddei, F.
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Jorgensen, F., Leach, S., Wilde, S. J., Davies, A., Stewart, G. S. A. B., Humphrey, T.
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Culham, D. E., Wood, J. M.
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Hilali, F., Ruimy, R., Saulnier, P., Barnabe, C., Lebouguenec, C., Tibayrenc, M., Andremont, A.
(2000). Prevalence of Virulence Genes and Clonality in Escherichia coli Strains That Cause Bacteremia in Cancer Patients. Infect. Immun.
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Mazel, D., Dychinco, B., Webb, V. A., Davies, J.
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Bonacorsi, S. P. P., Clermont, O., Tinsley, C., Le Gall, I., Beaudoin, J.-C., Elion, J., Nassif, X., Bingen, E.
(2000). Identification of Regions of the Escherichia coli Chromosome Specific for Neonatal Meningitis-Associated Strains. Infect. Immun.
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Johnson, J. R., Clabots, C.
(2000). Improved Repetitive-Element PCR Fingerprinting of Salmonella enterica with the Use of Extremely Elevated Annealing Temperatures. CVI
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Johnson, J. R., O'Bryan, T. T.
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Amor, K., Heinrichs, D. E., Frirdich, E., Ziebell, K., Johnson, R. P., Whitfield, C.
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