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1 ExPEC causes the vast majority of urinary tract infectio
2 ExPEC harboring a deletion of the gene encoding the mann
3 ExPEC strains are extracellular bacterial pathogens; the
4 of survival was used, four of six additional ExPEC strains, but not an E. coli laboratory strain, wer
6 trace the fate of PAC after they agglutinate ExPEC and follow PAC-ExPEC complexes in cell culture ass
10 nd 94% of samples, respectively; P<.001) and ExPEC contamination (4%, 19%, and 46%, respectively; P<.
11 ation of antimicrobial-resistant E. coli and ExPEC, which may represent a newly recognized group of m
12 O1 genomic islands among 828 human and avian ExPEC and commensal E. coli isolates was determined.
13 evidence that at least some human and avian ExPEC strains are highly similar to one another, and it
14 dherence phenotype resembling that of canine ExPEC prompted the present reevaluation of the canine-hu
16 used to compare the virulence of a clinical ExPEC isolate with its isogenic mutant impaired for the
17 bored by extraintestinal pathogenic E. coli (ExPEC) and encodes the genotoxin colibactin, is epidemio
18 known as extraintestinal pathogenic E. coli (ExPEC) and include human uropathogenic E. coli (UPEC) an
20 eages of extraintestinal pathogenic E. coli (ExPEC) and superseded serotyping for certain isolates wi
21 olate of extraintestinal pathogenic E. coli (ExPEC) leads to stable and long-term colonization of the
22 classic extraintestinal pathogenic E. coli (ExPEC) sequence types (STs) and case report ST131 househ
23 utant of extraintestinal pathogenic E. coli (ExPEC) strain CFT073 that could not synthesize the K2 ca
24 cialized extraintestinal pathogenic E. coli (ExPEC) strains and, increasingly, with antimicrobial res
26 ified as extraintestinal pathogenic E. coli (ExPEC), and even these isolates exhibited significantly
27 , termed extraintestinal pathogenic E. coli (ExPEC), that have a special ability to cause disease at
28 lones of extraintestinal pathogenic E. coli (ExPEC), which traditionally have been regarded primarily
31 extraintestinal pathogenic Escherichia coli (ExPEC) encode a variety of fitness and virulence factors
32 Extraintestinal pathogenic Escherichia coli (ExPEC) is the most common gram-negative bacterial pathog
33 Extraintestinal pathogenic Escherichia coli (ExPEC) reside in the enteric tract as a commensal reserv
34 Extracellular pathogenic Escherichia coli (ExPEC) strains are common causes of a variety of clinica
35 Extraintestinal pathogenic Escherichia coli (ExPEC) strains are typically benign within the mammalian
36 extraintestinal pathogenic Escherichia coli (ExPEC) strains, referred to as uropathogenic E. coli (UP
37 extraintestinal pathogenic Escherichia coli (ExPEC) with infectious potential for humans, presumed ho
38 extraintestinal pathogenic Escherichia coli (ExPEC), 63 environmental canine fecal deposits were eval
40 Extraintestinal pathogenic Escherichia coli (ExPEC), so named because this pathotype infects tissues
41 extraintestinal pathogenic Escherichia coli (ExPEC), such as avian pathogenic E. coli (APEC), and des
42 extraintestinal pathogenic Escherichia coli (ExPEC), which encodes the genotoxin colibactin, are inco
44 the chemotherapeutic drug cyclophosphamide, ExPEC translocates from the intestine to the lungs, live
46 ibactin synthesis), plus molecularly defined ExPEC status, were significantly associated with virulen
47 for further discrimination of the different ExPEC subpathotypes, serogroups, phylogenetic types, and
49 roles in pathogenesis are well described for ExPEC strains that cause urinary tract infections and me
50 s study indicates that FimH is important for ExPEC translocation, suggesting that the type 1 pilus is
51 intestinal tract is often a prerequisite for ExPEC-mediated pathogenesis, we set out to understand ho
58 d human isolates, including archetypal human ExPEC strains CFT073 (O6:K2:H1), 536 (O6:K15:H31), and J
61 es essentially indistinguishable from, human ExPEC strains, which implicates dogs and their feces as
63 virulence-associated genes typical of human ExPEC were prevalent among the canine fecal isolates.
64 similarities between APEC O1 and other human ExPEC strains belonging to the ST95 phylogenetic lineage
67 ping showed that some of the sequenced human ExPEC strains were more like APEC O1 than other human Ex
68 Mutation of either glpG or glpR impaired ExPEC growth in mucus and on plates containing the long-
69 asmids are found significantly more often in ExPEC, including ExPEC associated with human neonatal me
70 significantly more often in ExPEC, including ExPEC associated with human neonatal meningitis and avia
73 icantly associated with bacteremia, multiple ExPEC-associated virulence genes, and group B2, and with
74 lectively, we have shown that the ability of ExPEC to survive in macrophages is contingent upon the p
76 rulence in E. coli and that the evolution of ExPEC, which involves extensive horizontal transmission
78 port of a chemotherapy-based animal model of ExPEC translocation in cancerous mice, a system that can
79 deposits were evaluated for the presence of ExPEC by a combination of selective culturing, extended
84 he extraintestinal pathogenic versatility of ExPEC clones, which supports the use of an inclusive des
87 ld help us understand the virulence of other ExPEC strains and design more efficient infection contro
89 ived isolates of extraintestinal pathogenic (ExPEC) Escherichia coli, a common agent of sepsis and co
90 Fluorescent labeled PAC were able to promote ExPEC agglutination when observed with fluorescence micr
91 l pks island markers), and 12 other putative ExPEC virulence genes were newly sought by PCR among 131
95 that might contribute to the ability of some ExPEC strains to cause high-level bacteremia and meningi
98 In contrast, multiple known or suspected ExPEC virulence genes, including pap (P fimbriae), vat (
102 and transformed Caco-2 cells, we report that ExPEC strain CP9 binds to and invades the intestinal epi
103 e lines of evidence suggest that many of the ExPEC strains encountered in humans with urinary tract i
105 model of chemotherapy-induced translocation, ExPEC lacking fimH colonized at levels comparable to tha
107 mutant, and oxyRS mutants of other wild-type ExPEC strains, exhibited significantly increased in vitr
108 rred either in APEC O1 or in highly virulent ExPEC isolates, resulting in differences in pathogenicit
109 new avenues for defining mechanisms by which ExPEC strains colonize the mammalian gastrointestinal tr
112 everal virulence factors are associated with ExPEC, there is no core set of virulence factors that ca
113 eq) was performed to search for genes within ExPEC isolate F11 that are important for growth in intes
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