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1                                              S. epidermidis agr reporter strains were developed for e
2                                              S. epidermidis bacteria were cultured in vitro on the na
3                                              S. epidermidis biofilms preferentially form on abiotic s
4                                              S. epidermidis contains the cap operon, encoding the pol
5                                              S. epidermidis has the ability to attach to indwelling m
6                                              S. epidermidis isolates were collected from 104 patients
7 s of the infecting organisms, we examined 31 S. epidermidis NVE and 65 PVE isolates, as well as 21 is
8 phic demonstrated only two alleles in the 33 S. epidermidis isolates analyzed, corresponding to the p
9                              Analyzing 1,482 S. epidermidis genomes from 5 healthy individuals, we fo
10         A total of 1559 cultures yielded 565 S. epidermidis isolates; 254 of 548 typed isolates (46%)
11 ult Wistar rats [n = 6 sterile screws; n = 6 S. epidermidis-colonized screws; n = 26 C. acnes-coloniz
12 att site of both an isogenic S. aureus and a S. epidermidis recipient.
13       Limited information is available about S. epidermidis proteins that are expressed upon transiti
14                                Additionally, S. epidermidis sar fragments could restore hemolysin pro
15 am-positive pathogens, with activity against S. epidermidis that equals that of the currently prescri
16 nt antimicrobial inhibitory activity against S. epidermidis was maintained for 16 days.
17 tential targets for drug development against S. epidermidis infections.
18 n of adaptive immunity to protection against S. epidermidis challenge was complicated by a highly eff
19 ifferences related to the etiological agent (S. epidermidis in SAM; Staphylococcus aureus in AM), mil
20                The concentration of airborne S. epidermidis corresponded to a Raman peak at 732.5 cm(
21 idis accounted for only 1 death (0.5% of all S. epidermidis episodes) (P < 0.001).
22 d PMN migration into fibrin gels and allowed S. epidermidis to increase by approximately 300% in 4 h,
23 me, and performed expression profiling of an S. epidermidis biofilm.
24  more effective at killing P. aeruginosa and S. epidermidis at basic pH values (pH = 9) compared to a
25 ogenesis of biofilm-associated S. aureus and S. epidermidis and may contribute to the chronic nature
26               Both Staphylococcus aureus and S. epidermidis are capable of forming biofilm on biomate
27                    Staphylococcus aureus and S. epidermidis are major causes of infection related to
28 pletely inhibit drug-resistant S. aureus and S. epidermidis biofilms.
29  been identified that can bind S. aureus and S. epidermidis cells and are protective in an infant rat
30 ing epitopes on the surface of S. aureus and S. epidermidis cells.
31 latory differences between the S. aureus and S. epidermidis ferritins, as sefA expression in contrast
32                            The S. aureus and S. epidermidis genomes are syntenic throughout their len
33 bacterial load associated with S. aureus and S. epidermidis infection in an acute murine bacteremia m
34 tablished in vitro biofilms of S. aureus and S. epidermidis significantly more so than traditional an
35 lococci, above all Staphylococcus aureus and S. epidermidis, are the most frequent causes of biofilm-
36 cludes adhesins from Staphyloccus aureus and S. epidermidis.
37 th strains and genomic loci of S. aureus and S. epidermidis.
38 ted pathogens were Staphylococcus aureus and S. epidermidis.
39 ) of lauric acid on P. acnes, S. aureus, and S. epidermidis growth indicate that P. acnes is the most
40  log inactivation of E. coli, E. durans, and S. epidermidis, respectively, in clean water and seconda
41 e clearance of bacteremia by E. faecalis and S. epidermidis in mice.
42 promising biologic effects, in both HGFs and S. epidermidis.
43 us [MIC = 12.5-25.0 ug/ml (5.2-10.4 uM)] and S. epidermidis [MIC = 12.5 ug/ml (5.2 uM)], and moderate
44 nting a range of clonal complexes as well as S. epidermidis.
45 is study revealed that healthcare-associated S. epidermidis infection is remarkably clonal.
46 homologs found in other sequenced S. aureus, S. epidermidis and S. carnosus genomes.
47  biofilm formation by Staphylococcus aureus, S. epidermidis and Aggregatibacter actinomycetemcomitans
48 sing bacteria such as Staphylococcus aureus, S. epidermidis, and Pseudomonas aeruginosa, but without
49 gene was observed for Staphylococcus aureus, S. epidermidis, and S. haemolyticus as well as among mec
50 ystem was evaluated with five test bacteria: S. epidermidis, M. luteus, E. hirae, B. subtilis, and E.
51 potential use for normal commensal bacterium S. epidermidis to activate TLR2 signaling and induce ant
52                                         Both S. epidermidis and S. aureus Tpn catalyzed the conversio
53                     We also showed that both S. epidermidis bacterial particles and Embp can directly
54 be useful to limit formation of a biofilm by S. epidermidis.
55 aneuvers aimed at treating disease caused by S. epidermidis and related staphylococci.
56 the agr system enhances skin colonization by S. epidermidis using a porcine model.
57 n specifically prevents biofilm formation by S. epidermidis and methicillin-resistant S. aureus (MRSA
58                     Electricity generated by S. epidermidis may confer immediate innate immunity in a
59  modulins (PSMs) gamma and delta produced by S. epidermidis have an alpha-helical character and a str
60           By showing that PNAG production by S. epidermidis biofilm cells exacerbates host inflammato
61 t the production of PSMgamma and PSMdelta by S. epidermidis can benefit cutaneous immune defense by s
62 rnatant, reduced polysaccharide synthesis by S. epidermidis.
63 ination of quorum-sensing regulation used by S. epidermidis represents a surprising and unusual means
64 aphylococcal strains (S. aureus, S. capitis, S. epidermidis, S. haemolyticus, S. hominis, S. lugdunen
65 hole-cell lysates of S. aureus, S. carnosus, S. epidermidis, S. hominis, S. cohnii, S. lugdunensis, a
66 osthetic valves and intravascular catheters, S. epidermidis NVE is a virulent infection associated wi
67 riminate among previously well-characterized S. epidermidis clinical isolates.
68                                      Chronic S. epidermidis infections are often recalcitrant to trad
69                   Naive mice rapidly cleared S. epidermidis infections from blood and solid organs, e
70             Characterization of the clinical S. epidermidis isolates reveals in-host evolution over t
71 me-wide comparison of clinical and commensal S. epidermidis strains to identify putative virulence de
72 genic form of the ubiquitous human commensal S. epidermidis.
73         Representation of the skin commensal S. epidermidis also significantly increased during flare
74  show here the first evidence of a composite S. epidermidis pathogenicity island (SePI), the product
75 oprotease SepA is required for Aap-dependent S. epidermidis biofilm formation in static and dynamic b
76                                  We describe S. epidermidis clones that are highly resistant to antib
77  provide potential biomarkers to distinguish S. epidermidis infection from sterile postoperative infl
78 ared with 25% of rats challenged with either S. epidermidis O-47mut1 or O-47mut2 (P=.007).
79 age detection of Staphylococcus epidermidis (S. epidermidis) biofilm formation.
80  (E. durans) and Staphylococcus epidermidis (S. epidermidis) by PAA combined with UV concurrently (UV
81  both TthCsm and Staphylococcus epidermidis (S. epidermidis) Csm (SepCsm) cleave RNA transcripts, but
82 (S. aureus), and Staphylococcus epidermidis (S. epidermidis) with lauric acid yielded minimal inhibit
83 robes, including Staphylococcus epidermidis (S. epidermidis), a Gram-positive bacterium, live inside
84  (S. aureus) and Staphylococcus epidermidis (S. epidermidis).
85 uantification of Staphylococcus epidermidis (S. epidermidis).
86 produced isogenic deletion mutants for every S. epidermidis psm locus and a sequential deletion mutan
87 keratin and suggest that SdrF may facilitate S. epidermidis colonization of the skin.
88                                       As for S. epidermidis infections, determination of bacterial lo
89 uture) driveline exit site were cultured for S. epidermidis before VAD insertion and at 7 times after
90 tated, confirming that Embp is essential for S. epidermidis activity against viral infection.
91    The most significant virulence factor for S. epidermidis is its ability to form a biofilm, which r
92       To identify the proteins necessary for S. epidermidis attachment to collagen, we screened an ex
93 s, we analyzed the genome of biofilm-forming S. epidermidis, constructed a microarray representing it
94 ssembly, our findings indicate that Aap from S. epidermidis requires Zn(2+) as a catalyst that drives
95   Accumulation-associated protein (Aap) from S. epidermidis has been shown to be necessary and suffic
96 c followed by 9,960 CFUs and 9,900 CFUs from S. epidermidis wild type in BALB/c and CD-1, respectivel
97                 A cell surface fraction from S. epidermidis 0-47 grown in rabbit serum to mimic envir
98 rile nontoxic small molecule of <10 kDa from S. epidermidis conditioned culture medium (SECM), but no
99 t recognizing adhesive matrix molecules from S. epidermidis.
100 ctivity profiles in the AgrC-I receptor from S. epidermidis.
101                                 Furthermore, S. epidermidis isolates with high antimicrobial peptide-
102 ed Overnight Gram-Positive panels identified S. epidermidis strains accurately, but the panels perfor
103 rowth of P. aeruginosa, whereas impressively S. epidermidis did not grow at all when treated with a 5
104                                           In S. epidermidis, disparate environmental signals can affe
105                                           In S. epidermidis, polysaccharide intercellular adhesin (PI
106 rC interactions crucial for QS activation in S. epidermidis and advance the understanding of QS at th
107  in three S. aureus clinical isolates and in S. epidermidis.
108 n, and packaging of a novel bacteriophage in S. epidermidis FRI909, as well as attempts to mobilize t
109                    No significant changes in S. epidermidis load was found after one IVI.
110 ve and ACME-derived ADIs are compensatory in S. epidermidis.
111 ns Aap and SasG mediate biofilm formation in S. epidermidis and S. aureus, respectively.
112 ed protein Aap promotes biofilm formation in S. epidermidis, independently from the polysaccharide in
113 the extracellular lipase originally found in S. epidermidis 9, as a collagen-binding protein.
114 s, leukocidins, and leukotoxins not found in S. epidermidis.
115  least in part, mediates hemagglutination in S. epidermidis.
116  report here the cloning of a sar homolog in S. epidermidis.
117 rulence determinants have been identified in S. epidermidis, which are typically acquired through hor
118 esistance as associated with poor outcome in S. epidermidis ODRI.
119 t the in vivo biofilm infection phenotype in S. epidermidis is in accordance with the PSM biofilm str
120                       Integrated plasmids in S. epidermidis carry genes encoding resistance to cadmiu
121 olled by sar in S. aureus are not present in S. epidermidis, an examination of functional and structu
122                  The interpromoter region in S. epidermidis differs from its S. aureus counterpart, p
123 ting mecA-mediated beta-lactam resistance in S. epidermidis isolates.
124 fied mecA-mediated beta-lactam resistance in S. epidermidis Using mecA PCR as the gold standard, the
125   The major open reading frame within sar in S. epidermidis is highly homologous (84%) to the S. aure
126 a candidate target of balancing selection in S. epidermidis.
127 other bacterial pathogens, quorum sensing in S. epidermidis thus has a different role during biofilm
128   There is a single quorum-sensing system in S. epidermidis encoded by the agr operon.
129                   These data suggest that in S. epidermidis SaeR functions to regulate the transition
130 ts conjugation and plasmid transformation in S. epidermidis.
131                 There are three agr types in S. epidermidis strains, but only one of the autoinducing
132  on susceptibility to experimentally induced S. epidermidis disease.
133 ion and phenotypic features of the infecting S. epidermidis isolate with the clinical outcome for the
134  and other species of Cutibacteria inhibited S. epidermidis but did not inhibit biofilms by Pseudomon
135    This work provides detailed insights into S. epidermidis biofilm formation and architecture that i
136 athology induced by a subsequent intravenous S. epidermidis challenge, compared to priming with M10 c
137 i, we sequenced the DNA upstream of the 3-kb S. epidermidis sitABC operon, which Northern blot analys
138 crom into these gels in 6 h and did not kill S. epidermidis when the gels contained heat-inactivated
139 ated that specific secreted, surfactant-like S. epidermidis peptides--the beta subclass of phenol-sol
140                 Cytokine responses to a live S. epidermidis challenge are impaired in infants with LO
141 era generated in rabbits immunized with live S. epidermidis 0-47 or with biotin-labeled serum protein
142  peripheral whole blood stimulated with live S. epidermidis were analyzed by 11-plex immunoassay.
143                               In vitro, many S. epidermidis isolates stimulated nasal epithelia to pr
144 ARROWgard catheter when tested against MRSA, S. epidermidis, and E. faecalis (p < or = .002).
145 ex vivo antimicrobial activity against MRSA, S. epidermidis, and E. faecalis compared with the ARROWg
146 racterize the structures of the three native S. epidermidis AIP signals and five non-native analogs w
147 y differentiated mecA-positive and -negative S. epidermidis isolates, with categorical agreement (CA)
148 ribe the first report of a catalase-negative S. epidermidis strain.
149 e, evidence is provided that in PIA-negative S. epidermidis 1457Deltaica, the metalloprotease SepA is
150                                Until now, no S. epidermidis phage genome sequences have been reported
151 rved, in accordance with our finding that no S. epidermidis PSM produced amyloids.
152 fense capability and that S. aureus, but not S. epidermidis, triggers a PLA(2) response in the rabbit
153 ull thickness of the gels and to kill 80% of S. epidermidis in 4 h.
154 ckness of the gels in 6 h, and killed 90% of S. epidermidis in 6 h.
155    The CPID-2 panels identified 85 to 95% of S. epidermidis strains, 76 to 86% of S. hominis strains,
156 n significantly reduce in vitro adherence of S. epidermidis to immobilized collagen.
157    Anti-SdrF antibodies reduced adherence of S. epidermidis to keratin and keratinocytes.
158                           Subset analysis of S. epidermidis isolates 2 years after the study period s
159 s then tested using multiple applications of S. epidermidis supernatant, the repetitive inflammatory
160 ehD antibodies can inhibit the attachment of S. epidermidis to immobilized collagen.
161   To investigate potential CSF biomarkers of S. epidermidis shunt infection, we developed a rat model
162                  Blood and 1 to 1,000 CFU of S. epidermidis per ml in stationary or exponential phase
163 buffered saline, incubated with 10(6) CFU of S. epidermidis per ml, and cultured.
164 was confirmed to accelerate the clearance of S. epidermidis bacteremia, but TLR2(-/-)mice could still
165     PFGE demonstrated a predominant clone of S. epidermidis (major subtype A) which was 35.5 times mo
166 lator agr affects the biofilm development of S. epidermidis in an unexpected fashion and is likely in
167 ed BALB/cAnNCrl (BALB/c) male mice, doses of S. epidermidis O-47 wild type, its hemB mutant with stab
168 ent involved in the anti-influenza effect of S. epidermidis.
169  C. acnes may influence biofilm formation of S. epidermidis.
170 late, and the approximately 2.6-Mb genome of S. epidermidis RP62a, a methicillin-resistant biofilm is
171 tained high-resolution time-series images of S. epidermidis at 20-min intervals.
172                   All received injections of S. epidermidis on POD 10.
173 idis genome, new markers for invasiveness of S. epidermidis, and potential targets for drug developme
174 atly improve epidemiologic investigations of S. epidermidis.
175 a-lactam resistance in 100 human isolates of S. epidermidis (48 mecA-positive isolates and 52 mecA ne
176 aphylococcus xylosus, 3 distinct isolates of S. epidermidis, and all other tested human skin commensa
177           This work expands our knowledge of S. epidermidis agr system function and will aid future s
178 as essential for key virulence mechanisms of S. epidermidis, namely biofilm formation, colonization,
179 atty acid in the fermentation metabolites of S. epidermidis.
180    Our goal was to develop a murine model of S. epidermidis infection to identify potential vaccine t
181 ion, mediated by PIA, in the pathogenesis of S. epidermidis experimental CVC infection.
182 , mediated by PIA/HA, in the pathogenesis of S. epidermidis experimental CVC-associated infection.
183 , mediated by PIA/HA, in the pathogenesis of S. epidermidis experimental foreign body infection.
184 g the in vivo details of the pathogenesis of S. epidermidis infection.
185 e methods to investigate the pathogenesis of S. epidermidis infection.
186 s important role in the biofilm phenotype of S. epidermidis 1457, in which the Aap protein is process
187 abscess formation by different phenotypes of S. epidermidis in a foreign body infection model is most
188                   The taxonomic placement of S. epidermidis strain FRI909 was confirmed by a number o
189 ential vaccine targets for the prevention of S. epidermidis bacteremia.
190 roduction of PS/A and that the properties of S. epidermidis associated with initial bacterial adheren
191 pears to be perturbed by the Esp protease of S. epidermidis.
192  immunoreactive or serum binding proteins of S. epidermidis were identified by mass spectrometry.
193 eages and potential donors and recipients of S. epidermidis were identified in each case.
194 phenotype, the agr quorum-sensing regulon of S. epidermidis was characterized by a genomewide analysi
195  also found that a single B domain repeat of S. epidermidis 9491 retains the capacity to bind to type
196       Our study identifies a pivotal role of S. epidermidis in healthy maturation of the nasal microb
197 re supernatant also increased sensitivity of S. epidermidis to antibiotic killing under biofilm-formi
198                                  A series of S. epidermidis cell-wall mutants revealed that the cell
199 roscopy during both early and late stages of S. epidermidis biofilm formation, and we confirmed that
200 inactivation altered the metabolic status of S. epidermidis, resulting in a massive derepression of P
201        We created a bioluminescent strain of S. epidermidis and developed a subcutaneous catheter-rel
202                          A similar strain of S. epidermidis expressing an Aap-SpyCatcher chimera can
203          By colonizing mice with a strain of S. epidermidis in which the parallel beta-helix domain o
204 PGA was synthesized by all tested strains of S. epidermidis and a series of closely related coagulase
205 ily adsorbed out by PS/A-positive strains of S. epidermidis and recombinant strains of staphylococci
206         The results indicate that strains of S. epidermidis colonising the gut can cause serious path
207 rging evidence suggests that some strains of S. epidermidis may contribute to the pathogenesis of com
208 y therefore, the pathogenicity of strains of S. epidermidis which were isolated from the stool sample
209 to which the population genetic structure of S. epidermidis distinguishes commensal from pathogenic i
210 host tissues, contributing to the success of S. epidermidis as a pathogen.
211 disabling agr likely enhances the success of S. epidermidis during infection of indwelling medical de
212 ed significant alterations to the surface of S. epidermidis, and electron microscopy showed cellular
213  Streptococcus (GAS) but not the survival of S. epidermidis on mouse skin.
214             In contrast to the aps system of S. epidermidis, induction of the aps response in S. aure
215 e to exert a complete bactericidal effect on S. epidermidis and S. aureus strains and maintain steril
216 lin exhibited greater bactericidal effect on S. epidermidis than ceftriaxone.
217 e effect of these molecules was evaluated on S. epidermidis growth rate and HGF viability, gene expre
218 nd by propidium iodide influx experiments on S. epidermidis.
219 ytometry or immunofluorescence microscopy on S. epidermidis 0-47 grown in nutrient broth or in the pr
220       Eyes infected with either S. aureus or S. epidermidis demonstrated a significant increase in MP
221  Rabbits challenged with either S. aureus or S. epidermidis demonstrated a significant reduction in C
222 gene in 599 cultures containing S. aureus or S. epidermidis was 98.6% sensitive and 94.3% specific co
223 for 69 blood cultures with only S. aureus or S. epidermidis was concordant with susceptibility testin
224            The number of viable S. aureus or S. epidermidis was significantly reduced when incubated
225 istance in a species other than S. aureus or S. epidermidis.
226 o sequences adjacent to msrA on the original S. epidermidis plasmid was investigated.
227  capacity to degrade dermcidin, particularly S. epidermidis SepA.
228 e evidence that the murine epidermis permits S. epidermidis, a skin-specific bacterium, to shape the
229       The peak signatures in the polymorphic S. epidermidis locus were traced to an arcD-like gene ad
230                              PIA/HA-positive S. epidermidis 1457 was significantly more likely to cau
231 ultiple phenol-soluble modulins, a potential S. epidermidis virulence factor.
232 nistered in high-fat-fed mice, Hld-producing S. epidermidis significantly reduced markers associated
233 s of phenol-soluble modulins (PSMs)--promote S. epidermidis biofilm structuring and detachment in vit
234                   Furthermore, PGA protected S. epidermidis from high salt concentration, a key featu
235  (SasG) and accumulation-associated protein (S. epidermidis) promote biofilm formation through their
236 19 controls without enoxaparin; all received S. epidermidis injections on POD 10.
237 is work, we show in vitro that a recombinant S. epidermidis Csm1 cleaves single-stranded DNA and RNA
238 le S. epidermidis, and methicillin-resistant S. epidermidis with sensitivities of 95%, 80%, and 96%,
239 sistant S. aureus, and methicillin-resistant S. epidermidis.
240  Staphylococcus aureus, Meticillin-resistant S. epidermidis, Escherichia coli, Pseudomonas aeruginosa
241 s corresponding to five previously sequenced S. epidermidis genes were synthesized and then used to a
242       Importantly, PGA efficiently sheltered S. epidermidis from key components of innate host defens
243                                        Since S. epidermidis coexists with abundant Cutibacteria acnes
244 om 5 healthy individuals, we found that skin S. epidermidis isolates coalesce into multiple founder l
245 s from the closely related commensal species S. epidermidis and S. saprophyticus.
246                               In this study, S. epidermidis TCA cycle mutants were constructed, and t
247 ococcus epidermidis, methicillin-susceptible S. epidermidis, and methicillin-resistant S. epidermidis
248                     Here we demonstrate that S. epidermidis secretes poly-gamma-DL-glutamic acid (PGA
249                     We demonstrate here that S. epidermidis culture supernatants significantly suppre
250  PIA biosynthesis led us to hypothesize that S. epidermidis is "sensing" disparate environmental sign
251 rease in model clot heterogeneity shows that S. epidermidis can rupture a fibrin clot.
252                        Our data suggest that S. epidermidis adjusts its lifestyle to varying requirem
253       In conclusion, these data suggest that S. epidermidis bloodstream infection is cleared in a hig
254                   These results suggest that S. epidermidis in the nasal cavity may serve as a defenc
255  study is the first analysis suggesting that S. epidermidis isolates from patients with NVE constitut
256                                          The S. epidermidis fibrinogen (Fg)-binding adhesin SdrG is n
257                                          The S. epidermidis load in vitreous at the time of patients'
258                                          The S. epidermidis sodA gene expressed from a plasmid comple
259  SodM and SodA proteins of S. aureus and the S. epidermidis SodA protein exist as dimers.
260          Additionally, we show that both the S. epidermidis agonists and antagonists are active in S.
261  then used to amplify DNA sequences from the S. epidermidis strains by using PCR.
262 hat there are at least five Sir boxes in the S. epidermidis genome and at least three in the genome o
263 ence time and among the most elevated in the S. epidermidis genome.
264     To further understand the outputs of the S. epidermidis agr system, an RNAIII mutant was construc
265 the attachment or accumulation phases of the S. epidermidis biofilm phenotype.
266 udy revealed high genetic variability of the S. epidermidis genome, new markers for invasiveness of S
267  capacity and genetic diversification of the S. epidermidis isolates within the patient.
268                        The properties of the S. epidermidis PSMs suggest that they may contribute to
269       The deduced amino acid sequence of the S. epidermidis sodA was 92 and 76% identical to that of
270 no acid and nucleotide repeat regions of the S. epidermidis surface proteins SdrG and Aap show promis
271                              Remarkably, the S. epidermidis sar homolog interacts with an agr promote
272 emia despite taking antibiotics to which the S. epidermidis isolate is fully susceptible in vitro.
273  propionic, isobutyric or isovaleric acid to S. epidermidis inhibited biofilm formation and, similarl
274 ar response to STF and OspA-L in addition to S. epidermidis (PSM) Ags, and that engagement of TLR2 tr
275 These results demonstrate Aap contributes to S. epidermidis infection, which may in part be due to A
276 em to study the antigen-specific response to S. epidermidis, we demonstrated that skin colonization d
277 ha-toxin diminishes tolerogenic responses to S. epidermidis.
278 gests that care should be used when treating S. epidermidis infections with cross-inhibiting peptides
279 ence and a molecular characterization of two S. epidermidis phages, phiPH15 (PH15) and phiCNPH82 (CNP
280 ete genomic and molecular description of two S. epidermidis phages.
281 d intravenous catheter with either wild-type S. epidermidis 1457 or its isogenic PIA/HA-negative muta
282                                      Various S. epidermidis and Staphylococcus aureus strains were ex
283      Blood cytokine responses to an in vitro S. epidermidis challenge were similar between infected a
284 ecies identified as multidrug resistant were S. epidermidis, S. haemolyticus and S. hominis, whereas
285  were enriched in virulence factors, whereas S. epidermidis AD strains varied in genes involved in in
286 equire an initial colonization step in which S. epidermidis adheres to the implanted material.
287                                        While S. epidermidis typically causes indolent infections of p
288 tides, killing pathogenic competitors, while S. epidermidis itself proved highly resistant owing to i
289 as documented in 75% of rats challenged with S. epidermidis O-47, compared with 12.5% and 25% challen
290  acnes in a diverse microbial community with S. epidermidis can be beneficial to the host and demonst
291 nd CCL3 in the CSF of animals implanted with S. epidermidis-infected catheters compared to sterile co
292                      Catheter infection with S. epidermidis occurred in 32% of roll plates and 80% of
293 d catheters of 87.5% of rats inoculated with S. epidermidis O-47, compared with 25% of rats challenge
294                     All rats inoculated with S. epidermidis-colonized screws were culture-positive an
295 ed in mice challenged intraperitoneally with S. epidermidis biofilm cells of the PNAG-producing 9142
296 eus surface, of which three cross-react with S. epidermidis.
297 o 10(7) per ml were mixed in suspension with S. epidermidis at concentrations varying from 10(3) to 1
298  amyloid-like fibrils composed of Aap within S. epidermidis biofilms and demonstrated that a biologic
299 e was more common in rats inoculated with wt S. epidermidis, compared with AtlE- or PIA-deficient mut
300                               Wild-type (wt) S. epidermidis O-47 was significantly more likely to cau

 
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