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1 orally challenged with a clinical isolate of C. fetus.
2 901 for C. jejuni; m/z 10,726 and 11,289 for C. fetus.
3 juni, has not been previously documented for C. fetus.
4  of the entire 6.2-kb invertible region from C. fetus 23D revealed a probable 5.6-kb operon of four o
5  form a distinct phylotype between mammalian C. fetus and Campylobacter hyointestinalis.
6 chs of SCID mice were heavily colonized with C. fetus, and colonization was associated with the devel
7 e sequence identity with classical mammalian C. fetus, and there was evidence of recombination among
8                           The reservoirs for C. fetus are mainly cattle and sheep.
9         We found that C. jejuni has replaced C. fetus as the predominant Campylobacter species causin
10 ari, C. upsaliensis, C. hyointestinalis, and C. fetus), as well as C. helveticus and C. lanienae.
11             Two cases of quinolone-resistant C. fetus bacteremia were detected in HIV-infected patien
12 id not hybridize to DNAs from representative C. fetus, C. lari, C.
13           In total, these data indicate that C. fetus can use multiple sites within the FCR for its s
14                                          For C. fetus cells, expression of SLPs essentially eliminate
15                  Here we show that mammalian C. fetus consists of distinct evolutionary lineages, pri
16 ngs for SCID mice and also demonstrated that C. fetus could also infect the gastric mucosa of wild-ty
17 based evolutionary framework will facilitate C. fetus epidemiology research and the development of im
18 ity island and to gain further insights into C. fetus evolution, we examined several C. fetus genes i
19 into C. fetus evolution, we examined several C. fetus genes in 18 isolates.
20  but rather is an ancient constituent of the C. fetus genome, integral to its biology.
21                                    We detect C. fetus genomes in 8% of healthy human fecal metagenome
22 erize the sapA homologues further, a 65.9 kb C. fetus genomic region encompassing the sap locus from
23     Cloning and nucleotide sequencing of the C. fetus gyrA gene in the 2 resistant isolates demonstra
24 lonization of the cecum and colon tissues by C. fetus in SCID mice, no lesions were noted in these ti
25                     It is often assumed that C. fetus infection occurs in humans as a zoonosis throug
26       In order to develop an animal model of C. fetus infection, outbred ICR SCID mice were orally ch
27                                    Relapsing C. fetus infections in quinolone-treated HIV-infected pa
28 stigate the mechanisms involved in relapsing C. fetus infections, we compared SLP variation in 4 pair
29                 Thus, our work suggests that C. fetus is an unappreciated human intestinal pathobiont
30  although the major sap inversion pathway in C. fetus is RecA dependent, alternative lower-frequency,
31 ogrammed DNA inversion systems, inversion in C. fetus is recA dependent.
32 ogrammed DNA inversion systems, inversion in C. fetus is recA-dependent.
33 s have been developed to differentiate among C. fetus isolates for taxonomic and epidemiologic uses.
34 ifferent C. fetus strains, but for mammalian C. fetus isolates, genome size was well conserved (mean,
35 al sequence and attach to either type A or B C. fetus lipopolysaccharide in a serospecific manner.
36 s from 17 countries to provide evidence that C. fetus may have originated in humans around 10,500 yea
37                 Recent studies indicate that C. fetus reassorts a single promoter, controlling SLP ex
38       To explore this possibility, we cloned C. fetus recA and created mutant strains by marker rescu
39             Previous work has shown that the C. fetus sap inversion system is RecA dependent.
40                         To better understand C. fetus sap island diversity and variation mechanisms,
41                           E. coli expressing C. fetus sapA and sapCDEF secreted SapA, indicating that
42                                            A C. fetus sapD mutant neither produced nor secreted SLPs.
43            Analysis of the C termini of four C. fetus SLPs revealed conserved structures that are pot
44                                              C. fetus SLPs therefore are transported to the cell surf
45                                 In wild-type C. fetus strain 23D, all eight sapA homologues are locat
46 pregnant ewe with a recA mutant of wild-type C. fetus (strain 97-211) that expressed the 97-kDa SLP,
47 ther investigate the genetic diversity among C. fetus strains of different origins, subspecies, and s
48 and distribution of sapA homologues among 18 C. fetus strains of different subspecies, serotypes, and
49 s used for the RAPD analyses can distinguish C. fetus strains of reptile and mammal origin, five can
50 logenetic analysis of the core genomes of 23 C. fetus strains of the two subspecies showed a division
51 ons, we compared SLP variation in 4 pairs of C. fetus strains that infect humans; initial and follow-
52 howed varied genome patterns among different C. fetus strains, but for mammalian C. fetus isolates, g
53 hich are based on the closed genomes of five C. fetus strains.
54            In total, these data suggest that C. fetus subsp fetus strains of reptile and mammal origi
55 ammal origin, five can differentiate between C. fetus subsp. fetus and C. fetus subsp. venerealis str
56                 The fact that the serotype A C. fetus subsp. fetus and subsp. venerealis strains were
57 stics of three of the phenotypically defined C. fetus subsp. fetus strains to C. fetus subsp. venerea
58 ferentiate between C. fetus subsp. fetus and C. fetus subsp. venerealis strains, and four showed diff
59 lly defined C. fetus subsp. fetus strains to C. fetus subsp. venerealis strains, when considering the
60 ical evaluation of the clinical relevance of C. fetus subspecies identification by phenotypic assays.
61 ssays have been applied to differentiate the C. fetus subspecies, but none of these tests is consiste
62 t with the phenotypic classifications of the C. fetus subspecies.
63 e general population is regularly exposed to C. fetus through foods of animal origin, cross-contamina
64 at most two structural genes, the ability of C. fetus to use this phenomenon to express one of multip
65 single sapA promoter, and that for variation C. fetus uses a mechanism of DNA rearrangement involving
66  in the sap locus, play an important role in C. fetus virulence.
67 fined the core genome and accessory genes of C. fetus, which are based on the closed genomes of five
68         The surface-layer proteins (SLPs) of C. fetus, which are critical in virulence, undergo high-

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