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2 ere ectopically expressed, the expression of coagulase, a sae target with low affinity for phosphoryl
3 pigmentation, and decreased hemolysis and/or coagulase activity are periodically isolated by the clin
6 gnificantly alter the expression patterns of coagulase and alpha-hemolysin, two well-known sae target
9 ting with 125I-fibrinogen, we could identify coagulase and an additional unidentified 52-kDa protein
10 hibitory clindamycin stimulates synthesis of coagulase and fibronectin binding protein B, also at the
11 genes encoding alkaline shock protein 23 and coagulase and have demonstrated SigB and RsbW dependence
12 gy, tests for clumping factor, and tests for coagulase and urease activities and were also tested wit
13 s, assembly of protective fibrin shields via coagulases and protein A-mediated B cell superantigen ac
16 he increased expression and transcription of coagulase as shown by Western (immunoblot) and Northern
17 ons were regulated by SaeRS and dependent on coagulase-catalyzed conversion of fibrinogen into fibrin
19 protein A (spa), gamma hemolysin (hlg), and coagulase (coa) were also located on the map by PFGE and
20 ulated surface determinants (IsdA and IsdB), coagulase (Coa), and von Willebrand factor binding prote
22 nfection, Staphylococcus aureus secretes two coagulases (Coa and von Willebrand factor binding protei
23 the variable prothrombin binding portion of coagulases confer type-specific immunity through the neu
24 tudy, we use a S. aureus mutant lacking both coagulases (Deltacoa/vwb) and dabigatran, a pharmacologi
25 ty and its relationship to the expression of coagulase (encoded by coa) and clumping factor (encoded
26 ureus was identified from all media by slide coagulase, exogenous DNase, and mannitol fermentation as
29 agment length polymorphism (PCR-RFLP) of the coagulase gene and pulsed-field gel electrophoresis (PFG
30 d based on improved PCR amplification of the coagulase gene and restriction fragment length polymorph
31 ally, strains were subtyped according to the coagulase gene in order to strengthen discriminatory pow
34 the genomes of different S. aureus isolates, coagulase gene sequences are variable, and this has been
35 irulence factors such as alpha-hemolysin and coagulase; however, the molecular mechanism of this sign
36 hese findings emphasize the critical role of coagulase in staphylococcal escape from opsonophagocytic
41 ased risk of nosocomial bacterial sepsis and coagulase negative staphylococcal infections, and thus s
43 predominantly isolated pathogen, followed by Coagulase negative staphylococci (CoNS) (33.5%) and Kleb
47 ssociated with Klebsiella pneumoniae whereas Coagulase negative Staphylococci and Bacillus spp. are c
50 ccus viridians, Streptococcus pneumoniae and Coagulase negative Staphylococci in endophthalmitis diag
51 P. aeruginosa and E. coli in dacryocystitis; Coagulase negative Staphylococci, Pseudomonas aeruginosa
52 s far as this review, Staphylococcus aureus, Coagulase negative Staphylococci, Streptococcus pneumoni
55 ed among the S. aureus isolates; however, 10 coagulase-negative isolates were MecA+ but oxacillin sen
57 validated by correctly identifying 36 of 37 coagulase-negative staphylococcal (CoNS) isolates identi
58 caprae was the cause of 6 of 18 episodes of coagulase-negative staphylococcal bacteremia, was the mo
59 ive quantitative blood cultures and definite coagulase-negative staphylococcal bloodstream infection.
63 has been implicated in a large proportion of coagulase-negative staphylococcal infections in very-low
66 ed non-prosthetic joint infection-associated coagulase-negative staphylococcal isolates were icaA pos
68 mong which filamentous fungi (25, 39.1%) and coagulase-negative staphylococci (14, 21.9%) comprised a
70 ms causing CLABSI in oncology locations were coagulase-negative staphylococci (16.9%), Escherichia co
71 Staphylococcus epidermidis (MSSE) (9), other coagulase-negative staphylococci (19), Streptococcus sal
73 The most frequent causal microorganisms were coagulase-negative staphylococci (24%), followed by Stap
76 organism (128 patients [23.0%]), followed by coagulase-negative staphylococci (94 patients [16.9%]).
77 , (ii) distinguish between S. aureus and the coagulase-negative staphylococci (CNS) (based on amplifi
81 s and 100 isolates of erythromycin-resistant coagulase-negative staphylococci (CNS) were examined by
83 lococcus epidermidis, Staphylococcus aureus, coagulase-negative staphylococci (CNS), Peptostreptococc
85 The most common organisms identified were Coagulase-negative Staphylococci (CoNS) [65.9% (91/138)]
86 ) to accurately differentiate S. aureus from coagulase-negative staphylococci (CoNS) and other Gram-p
87 investigating issues related to isolation of coagulase-negative staphylococci (CoNS) and other skin m
89 gh horizontal gene transfer originating from coagulase-negative staphylococci (CoNS) and through clon
92 microdilution and disk diffusion testing of coagulase-negative staphylococci (CoNS) by using a PCR a
94 he presence of secreted cytotoxic factors of coagulase-negative staphylococci (CoNS) from bovine clin
95 Differentiating Staphylococcus aureus from coagulase-negative staphylococci (CoNS) is important in
96 used to determine the clinical importance of coagulase-negative staphylococci (CoNS) is isolation of
97 P67 card for detecting methicillin-resistant coagulase-negative staphylococci (CoNS) is not known.
98 sis is an aggressive, virulent member of the coagulase-negative staphylococci (CoNS) that is responsi
99 Unbiased species-level identification of coagulase-negative staphylococci (CoNS) using matrix-ass
100 .01 for detection of oxacillin resistance in coagulase-negative staphylococci (CoNS) was compared to
101 s for detection of Staphylococcus aureus and coagulase-negative staphylococci (CoNS) were 99.5% (217/
102 inical isolates of Staphylococcus aureus and coagulase-negative staphylococci (CoNS) were determined
104 spersal of S. aureus, a 1.4-fold increase in coagulase-negative staphylococci (CoNS), and a 3.9-fold
105 methicillin-resistant S. aureus (MRSA), and coagulase-negative staphylococci (CoNS), including methi
106 and 53 strains of Staphylococcus aureus and coagulase-negative staphylococci (CoNS), respectively.
107 it ocular isolates of Staphylococcus aureus, coagulase-negative staphylococci (CoNS), Streptococcus p
110 lar for infections caused by enterococci and coagulase-negative staphylococci (CoNS; adjusted SHR, 0.
113 ruginosa (2 of 4), streptococci (2 of 5), or coagulase-negative staphylococci (none of 8) (P = 0.02).
114 More staphylococci (P < 0.05), especially coagulase-negative staphylococci (P < 0.05), and yeasts
115 < 0.001), Staphylococcus aureus (P = 0.003), coagulase-negative staphylococci (P = 0.008), gram-negat
116 N anaerobic bottle, while significantly more coagulase-negative staphylococci (P = 0.01), Streptococc
117 and streptococci slightly declined, whereas coagulase-negative staphylococci and enterococci consist
118 enced recurrence in this study (isolation of coagulase-negative staphylococci and inadequate duration
121 ganisms; the species cultured were typically coagulase-negative staphylococci and were associated wit
126 species identification of blood isolates of coagulase-negative staphylococci as a predictor of the c
127 ); (ii) controlled cultural findings showing coagulase-negative staphylococci as the most common isol
128 s more likely to have poor final acuity than coagulase-negative staphylococci cases (adjusted OR, 11.
131 temic infections is usually required because coagulase-negative staphylococci have become increasingl
133 8), Candida albicans in 5.8% (26/443), other coagulase-negative staphylococci in 6.0% (27/448), Propi
134 ferentiate between Staphylococcus aureus and coagulase-negative staphylococci in blood cultures growi
135 or determining beta-lactam susceptibility in coagulase-negative staphylococci in our laboratory.
137 days for S. aureus infection vs. 14 days for coagulase-negative staphylococci infection [p < 0.001]).
138 olonisation of indwelling medical devices by coagulase-negative staphylococci is a prevalent risk in
139 iated with prosthetic joint infection and 23 coagulase-negative staphylococci isolated from noninfect
141 eliability of routine sensitivity testing in coagulase-negative staphylococci often lead to the use o
143 oximately 60% of the samples (730) contained coagulase-negative staphylococci or nonstaphylococci as
144 species of Acinetobacter, Enterobacter, and coagulase-negative staphylococci recovered from the hand
148 Similar numbers of consecutive patients with coagulase-negative staphylococci were analyzed for compa
150 nstitutional rates of 73% contamination when coagulase-negative staphylococci were identified, 67.6%
152 cocci, and 11/42 (26%) methicillin-resistant coagulase-negative staphylococci were mupirocin resistan
155 n pathogens were associated with device use: coagulase-negative staphylococci with central lines, P.
156 eudomonas with piperacillin (1 of 28, 3.6%), coagulase-negative staphylococci with oxacillin (2 of 74
157 isolate each of Propionibacterium acnes and coagulase-negative staphylococci) in FAN bottles, wherea
158 aureus and 56 [31.6% {95% CI, 24.9%-39.0%}] coagulase-negative staphylococci); and a high prevalence
160 tive bacteria, 40 Staphylococcus aureus, 152 coagulase-negative staphylococci, 28 streptococci, 22 en
162 ssociated infections are currently caused by coagulase-negative staphylococci, a pathogen that incite
163 isms that are often considered contaminants (coagulase-negative staphylococci, aerobic and anaerobic
164 isolates, 3/16 (19%) methicillin-susceptible coagulase-negative staphylococci, and 11/42 (26%) methic
166 lates were Staphylococcus epidermidis, other coagulase-negative Staphylococci, and Corynebacterium sp
167 d isolates, including Staphylococcus aureus, coagulase-negative staphylococci, Enterococcus faecalis,
169 increased isolation of Enterococcus species, coagulase-negative staphylococci, intrinsically antibiot
170 epidermidis and a series of closely related coagulase-negative staphylococci, most of which are oppo
171 -1), enterotoxin, and other superantigens by coagulase-negative staphylococci, no associated pathogen
172 negative bacterial rods and three species of coagulase-negative staphylococci, recovered from both th
175 methicillin-resistant Staphylococcus aureus, coagulase-negative staphylococci, vancomycin-resistant e
188 olate was Propionibacterium acnes (11/26) vs coagulase-negative Staphylococcus (57/92); and 4) patien
190 ely 30 Staphylococcus aureus isolates and 20 coagulase-negative staphylococcus (CoNS) isolates in a p
191 disk and MIC breakpoints, the CLSI M100-S25 coagulase-negative Staphylococcus (CoNS) oxacillin MIC b
192 and 9 (2.5%) were identified by StaphPlex as coagulase-negative Staphylococcus (CoNS), methicillin-re
196 on at both DEI (70%) and LAC+USC (68%), with coagulase-negative Staphylococcus being the most common
197 tes, the most commonly isolated organism was coagulase-negative Staphylococcus both at baseline (73%)
198 organism (30.6%), but the number of isolated coagulase-negative Staphylococcus cases increased signif
199 significantly decreased the number of nasal coagulase-negative Staphylococcus compared with saline c
203 aphylococcal bacteremia, was the most common coagulase-negative staphylococcus recovered from the nar
205 llin-resistant Staphylococcus aureus (4.4%), coagulase-negative Staphylococcus species (15.3%), Strep
206 vestigations revealing no microorganism or a coagulase-negative Staphylococcus species (CNSP), and fu
209 d methicillin-susceptible S. aureus species, coagulase-negative Staphylococcus species, and other cli
211 gnificantly more Bacillus spp. (P < 0.0001), coagulase-negative Staphylococcus spp. (P < 0.0001), and
212 es of Staphylococcus aureus (P = 0.0113) and coagulase-negative Staphylococcus spp. (P = 0.0029) than
213 tream infections (septic episodes) caused by coagulase-negative Staphylococcus spp. (P = 0.0146).
214 ty-nine clinical staphylococcal isolates (58 coagulase-negative Staphylococcus spp. [CoNS] and 41 Sta
215 ion, using breakpoints for human isolates of coagulase-negative Staphylococcus spp., had low sensitiv
216 fied as 10 MRSA strains, 10 MSSA strains, 12 coagulase-negative Staphylococcus strains, and 8 Microco
221 easts, Actinobacillus actinomycetemcomitans, coagulase-negative Staphylococcus, Campylobacter rectus,
222 nd II, and vitreous cultures for infections (coagulase-negative Staphylococcus, Candida, Fusarium, an
223 ye preparations demonstrated the presence of coagulase-negative Staphylococcus, Streptococcus type al
225 (P < 0.001), S. aureus isolates (P < 0.001), coagulase-negative staphyococci (P = 0.003), and total o
229 d-phase fibrinogen, clumping factor, but not coagulase, plays a major role in binding to immobilized
233 on that had previously been characterized as coagulase-positive S. hyicus based on phenotypic species
234 Although Staphylococcus intermedius and coagulase-positive species of staphylococci are reported
236 ection control decisions requires that these coagulase-positive staphylococci are accurately identifi
239 , partially controls exoprotein synthesis in coagulase-positive Staphylococcus aureus by modulating t
241 phenotypic properties of beta-hemolysis and coagulase positivity allowed the clinical isolates to ma
242 acing between promoter elements in P1 or the coagulase promoter was altered to the optimal spacing of
249 an S. aureus strain with genetic deletion of coagulases, survival of mice improved, highlighting the
251 h (API) (bioMerieux, Durham, N.C.), the tube coagulase test (TCT) read at 4 h, and peptide nucleic ac
253 Staphaurex Plus, Staphyloslide, and the tube coagulase test for the identification of staphylococcal
256 o difference in the performance of the slide coagulase test or in susceptibility testing performed on
261 uding VWF-binding protein (vWbp), a secreted coagulase that activates the host's prothrombin to gener
262 protection against challenge with different coagulase-type S. aureus strains in mice was derived.
264 us hyicus and Staphylococcus agnetis are two coagulase-variable staphylococcal species that can be is
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