ライフサイエンスコーパス: S. lugdunensis

1 S. lugdunensis binding to VWF, collagen, and endothelial

2 S. lugdunensis binds directly to VWF, which proved to be

3 S. lugdunensis displayed a shorter course of infection a

4 S. lugdunensis is increasingly being recognized as a cau

5 S. lugdunensis is increasingly being recognized as a cau

6 S. lugdunensis IsdP was found to be iron regulated and c

7 S. lugdunensis may be an unrecognized yet infrequent cau

8 sis isolated in pure culture; 29 (94%) of 31 S. lugdunensis isolates were part of mixed nonpathogenic

9 identifying the reference strain and all 47 S. lugdunensis isolates without inappropriate amplificat

10 enge isolates that totaled 175 S. aureus, 70 S. lugdunensis, 121 E. faecalis, 100 E. faecium, 578 Ent

11 th antibiotics that may be effective against S. lugdunensis.

12 icaADBC homologues were found in all S. lugdunensis isolates tested, although the locus organ

13 in S. aureus compared to S. epidermidis and S. lugdunensis PJI, and CCL11 detected at higher levels

14 ) of 500 isolates of CoNS were identified as S. lugdunensis.

15 itral valve endocarditis, were identified as S. lugdunensis.

16 Oxacillin BMD using S. aureus/S. lugdunensis breakpoints yielded the highest VMEs at 1

17 and BMD results interpreted using S. aureus/S. lugdunensis breakpoints, the CA was 97.6% and 96.2%,

18 the iron acquisition mechanisms employed by S. lugdunensis, especially during infection of the mamma

19 ophores and catecholamine stress hormones by S. lugdunensis required the presence of the sst-1 transp

20 osus, S. epidermidis, S. hominis, S. cohnii, S. lugdunensis, and S. haemolyticus, we identified an ap

21 say that is able to definitively distinguish S. lugdunensis from other staphylococci.

22 on-heme iron acquisition systems also enable S. lugdunensis to cause human infection.

23 It remains unclear what factors enable S. lugdunensis to transition from a skin commensal to an

24 ion and the resulting release of VWF enabled S. lugdunensis to bind and colonize the heart valves.

25 he assay was both sensitive and specific for S. lugdunensis, correctly identifying the reference stra

26 tes were >90% with exception of C. freundii, S. lugdunensis, E. faecalis, S. anginosus and S. constel

27 ved between cadD and the cadB-like gene from S. lugdunensis, but no significant similarity was found

28 S. epidermidis, S. haemolyticus, S. hominis, S. lugdunensis, S. schleiferi, S. simulans, and S. warne

29 gether these findings offer insight into how S. lugdunensis fulfills its nutritional requirements whi

30 PNAG was not detected in S. lugdunensis extracts by immunoblotting with an anti-d

31 icaR was not detected in S. lugdunensis, but a novel open reading frame with puta

32 he genetic presence of icaADBC homologues in S. lugdunensis isolates, PNAG is not a major component o

33 hophysiologically relevant heme oxygenase in S. lugdunensis.

34 germ agglutinin showed a paucity of PNAG in S. lugdunensis biofilms, but abundant extracellular prot

35 To cause endovascular infections, S. lugdunensis requires mechanisms to overcome shear str

36 s species isolates (S. aureus, 211 isolates; S. lugdunensis, 3 isolates; and Staphylococcus spp., 444

37 CLSI BMD MIC for 98.9% of S. aureus, 100% of S. lugdunensis, 98.3% of E. faecalis, 100% of E. faecium

38 In vivo adhesion of S. lugdunensis was evaluated in a mouse microvasculature

39 e laboratory and clinical characteristics of S. lugdunensis PJIs seen at the Mayo Clinic in Rochester

40 film formation properties of a collection of S. lugdunensis clinical isolates.

41 There were 28 episodes of S. lugdunensis PJIs in 22 patients; half of those patien

42 for the routine and timely identification of S. lugdunensis in the clinical microbiology laboratory.

43 se data indicate that nearly all isolates of S. lugdunensis are susceptible to narrow-spectrum antimi

44 wed to evaluate the clinical significance of S. lugdunensis isolation, the antimicrobial agents presc

45 Many types of S. lugdunensis infection, including native valve endocar

46 of the mesenteric circulation, VWF recruited S. lugdunensis to the vessel wall.

47 E caused by Staphylococcus epidermidis (SE), S. lugdunensis (SL), and other CoNS.

48 ining uncommon targets (e.g., Listeria spp., S. lugdunensis, vanB-positive Enterococci) were included

49 M. sciuri) and 11 Non-aureus staphylococci (S. lugdunensis) isolates.

50 y to other coagulase-negative staphylococci, S. lugdunensis bound to VWF under flow, thus enabling it

51 Unique among the known Isd systems, S. lugdunensis contains a gene encoding a putative autol

52 es Staphylococcus aureus and CoNS other than S. lugdunensis and determines MecA-dependent resistance

53 In this study, we establish that S. lugdunensis expresses an iron-regulated IsdG-family h

54 Here we show that S. lugdunensis can usurp hydroxamate siderophores and st

55 hile invading host tissues and establish the S. lugdunensis Isd system as being involved in heme-iron

56 Our data suggest that the S. lugdunensis biofilm matrix contains proteinaceous fac

57 trains), for two Staphylococcus warneri, two S. lugdunensis, and two S. saprophyticus strains MICs we

58 In no case was S. lugdunensis isolated in pure culture; 29 (94%) of 31

59 nfection of mice, we demonstrated that while S. lugdunensis does not cause overt illness, it does col

60 The medical records of 62 patients from whom S. lugdunensis was isolated, including 31 penicillin-sus

61 This mechanism explains why S. lugdunensis causes more-aggressive infections, includ

62 face determinant (Isd) system encoded within S. lugdunensis.