ライフサイエンスコーパス: C. fetus

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 apeutic options for consideration in serious C. fetus infections, pending susceptibility results.

29 stigate the mechanisms involved in relapsing C. fetus infections, we compared SLP variation in 4 pair

30 C. fetus interpretive criteria are needed to aid clinici

31 Thus, our work suggests that C. fetus is an unappreciated human intestinal pathobiont

32 although the major sap inversion pathway in C. fetus is RecA dependent, alternative lower-frequency,

33 ogrammed DNA inversion systems, inversion in C. fetus is recA dependent.

34 ogrammed DNA inversion systems, inversion in C. fetus is recA-dependent.

35 s have been developed to differentiate among C. fetus isolates for taxonomic and epidemiologic uses.

36 C. fetus isolates from patients treated at Mayo Clinic a

37 e reviewed antimicrobial susceptibilities of C. fetus isolates tested at a tertiary care center and r

38 ifferent C. fetus strains, but for mammalian C. fetus isolates, genome size was well conserved (mean,

39 and meropenem demonstrated favorable MICs in C. fetus isolates.

40 al sequence and attach to either type A or B C. fetus lipopolysaccharide in a serospecific manner.

41 s from 17 countries to provide evidence that C. fetus may have originated in humans around 10,500 yea

42 Recent studies indicate that C. fetus reassorts a single promoter, controlling SLP ex

43 To explore this possibility, we cloned C. fetus recA and created mutant strains by marker rescu

44 Previous work has shown that the C. fetus sap inversion system is RecA dependent.

45 To better understand C. fetus sap island diversity and variation mechanisms,

46 E. coli expressing C. fetus sapA and sapCDEF secreted SapA, indicating that

47 A C. fetus sapD mutant neither produced nor secreted SLPs.

48 Analysis of the C termini of four C. fetus SLPs revealed conserved structures that are pot

49 C. fetus SLPs therefore are transported to the cell surf

50 In wild-type C. fetus strain 23D, all eight sapA homologues are locat

51 pregnant ewe with a recA mutant of wild-type C. fetus (strain 97-211) that expressed the 97-kDa SLP,

52 ther investigate the genetic diversity among C. fetus strains of different origins, subspecies, and s

53 and distribution of sapA homologues among 18 C. fetus strains of different subspecies, serotypes, and

54 s used for the RAPD analyses can distinguish C. fetus strains of reptile and mammal origin, five can

55 logenetic analysis of the core genomes of 23 C. fetus strains of the two subspecies showed a division

56 ons, we compared SLP variation in 4 pairs of C. fetus strains that infect humans; initial and follow-

57 howed varied genome patterns among different C. fetus strains, but for mammalian C. fetus isolates, g

58 hich are based on the closed genomes of five C. fetus strains.

59 In total, these data suggest that C. fetus subsp fetus strains of reptile and mammal origi

60 ammal origin, five can differentiate between C. fetus subsp. fetus and C. fetus subsp. venerealis str

61 The fact that the serotype A C. fetus subsp. fetus and subsp. venerealis strains were

62 stics of three of the phenotypically defined C. fetus subsp. fetus strains to C. fetus subsp. venerea

63 ferentiate between C. fetus subsp. fetus and C. fetus subsp. venerealis strains, and four showed diff

64 lly defined C. fetus subsp. fetus strains to C. fetus subsp. venerealis strains, when considering the

65 ical evaluation of the clinical relevance of C. fetus subspecies identification by phenotypic assays.

66 ssays have been applied to differentiate the C. fetus subspecies, but none of these tests is consiste

67 t with the phenotypic classifications of the C. fetus subspecies.

68 e general population is regularly exposed to C. fetus through foods of animal origin, cross-contamina

69 at most two structural genes, the ability of C. fetus to use this phenomenon to express one of multip

70 single sapA promoter, and that for variation C. fetus uses a mechanism of DNA rearrangement involving

71 in the sap locus, play an important role in C. fetus virulence.

72 associated with gastrointestinal signs, and C. fetus was associated with secondary localizations.

73 fined the core genome and accessory genes of C. fetus, which are based on the closed genomes of five

74 The surface-layer proteins (SLPs) of C. fetus, which are critical in virulence, undergo high-