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1 coccus epidermidis, Candida albicans, and K. kingae.
2 omologs play important roles in mediating K. kingae adherence.
3 t study, we examined interactions between K. kingae and cultured respiratory epithelial cells and obs
4 genetic requirements for encapsulation in K. kingae and demonstrate an atypical organization of capsu
5 model for understanding disease caused by K. kingae and for elucidating diagnostic parameters in huma
6 ifferences in PilC1 and PilC2 function in K. kingae and provide insights into the biology of the PilC
7 spite the increasing recognition of Kingella kingae as an important pathogen of early childhood, the
8 infection and a selective disadvantage on K. kingae at later stages in the pathogenic process.
9 pB (kpsS)-like gene, and the csaA gene in K. kingae capsule production.
10                   A total of 32 different K. kingae clones were identified by PFGE, of which 5 (B, H,
11    Cell-free extracts prepared from Kingella kingae colony biofilms were found to inhibit biofilm for
12                       The pathogenesis of K. kingae disease begins with bacterial adherence to respir
13  associated with clinical presentation of K. kingae disease in humans and suggests that the toxin con
14 les for this toxin in the pathogenesis of K. kingae disease include breaching of the epithelial barri
15                       The pathogenesis of K. kingae disease is believed to begin with colonization of
16       Despite the increasing frequency of K. kingae disease, little is known about the mechanism by w
17  pili may confer a selective advantage on K. kingae early in infection and a selective disadvantage o
18  to determine the genetic determinants of K. kingae encapsulation.
19          The comprehensive description of K. kingae evolution would help to detect new emerging clone
20                                  Although K. kingae exhibits noteworthy genetic heterogeneity, a limi
21                         We concluded that K. kingae expresses an RTX toxin that has wide cellular spe
22                 Previous work showed that K. kingae expresses long surface fibers that vary in surfac
23            Previous work established that K. kingae expresses type IV pili that mediate adherence to
24         Recent work has demonstrated that K. kingae expresses type IV pili that mediate adherence to
25 at the biofilm inhibition activity in the K. kingae extract was due to polysaccharide.
26                        A cluster of three K. kingae genes encoding UDP-galactopyranose mutase (ugm) a
27                   Upon examination of the K. kingae genome, we identified two genes in physically sep
28 conducted to determine the association of K. kingae genotypes with specific clinical syndromes and th
29 m hominis, Eikenella corrodens, and Kingella kingae (HACEK) clinical isolates and 20 Haemophilus infl
30 Staphylococcus aureus treatment and Kingella kingae identification are changing the approach to skin
31                                     Kingella kingae is a commensal of the upper respiratory tract tha
32                                     Kingella kingae is a common cause of invasive disease in young ch
33                                     Kingella kingae is a gram-negative bacterium that colonizes the r
34                                     Kingella kingae is a gram-negative bacterium that is being recogn
35                                     Kingella kingae is a human oral bacterium that can cause diseases
36                                     Kingella kingae is a human oral bacterium that can cause infectio
37                                     Kingella kingae is a member of the Neisseriaceae and is being rec
38 istant Staphylococcus aureus exists.Kingella kingae is a more prevalent cause of osteoarticular infec
39                                     Kingella kingae is also increasingly identified as a cause of ost
40                                     Kingella kingae is an emerging bacterial pathogen that is being r
41                                     Kingella kingae is an emerging bacterial pathogen that is increas
42                            Although Kingella kingae is the most common etiology of osteoarticular inf
43 may serve in the initial investigation of K. kingae outbreaks.
44 d a paracentesis on himself and developed K. kingae peritonitis and bacteremia.
45  mutant strains revealed that both of the K. kingae PilC homologs are essential for a wild-type level
46 of either PilC1 or PilC2 is necessary for K. kingae piliation and bacterial adherence.
47                                           K. kingae produces a toxin of the RTX group, RtxA.
48  The disruption of either rpoN or pilR in K. kingae resulted in a marked reduction in the level of tr
49                         Disruption of the K. kingae RTX locus resulted in a loss of cytotoxicity for
50  current study, we examined the genome of K. kingae strain 269-492 and identified homologs of the rpo
51  of RtxA in disease pathogenesis in vivo, K. kingae strain PYKK081 and its isogenic RtxA-deficient st
52 draft genome sequence of septic arthritis K. kingae strain PYKK081.
53                                           K. kingae strains also show significant association with sp
54 he largest intercontinental collection of K. kingae strains to date.
55              A collection of 181 invasive K. kingae strains, isolated between 1991 and 2012 from Isra
56       PilA1 is the major pilus subunit in K. kingae type IV pili and is essential for pilus assembly.
57 lop a better understanding of the role of K. kingae type IV pili during colonization and invasive dis
58 These data suggest that the regulation of K. kingae type IV pilus expression is complex and multilaye
59 ur results demonstrate that RtxA is a key K. kingae virulence factor.

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