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1 roteus-like (MR/P) fimbriae of uropathogenic Proteus mirabilis.
2 philus influenzae, Bacteroides fragilis, and Proteus mirabilis.
3 een of the isolates were E. coli and one was Proteus mirabilis.
4 ion, is a virulence factor for uropathogenic Proteus mirabilis.
5 e is insufficient for protective activity in Proteus mirabilis.
6 he presence of collagenolytic E faecalis and Proteus mirabilis.
7 acid decarboxylase that inhibits swarming in Proteus mirabilis.
8 d for swarming in the urinary tract pathogen Proteus mirabilis.
9 ity to a putrescine-deficient speA mutant of Proteus mirabilis.
10 es in Klebsiella spp., Escherichia coli, and Proteus mirabilis.
11 important virulence factor of uropathogenic Proteus mirabilis.
12 toxin to prevent urinary tract infection by Proteus mirabilis.
13 cloacae complex, 18 Serratia marcescens, 12 Proteus mirabilis, 10 Citrobacter koseri, 9 Citrobacter
14 ifferentiation of Klebsiella pneumoniae from Proteus mirabilis 16S rRNA target sequences differing by
15 r baumannii (5%), Enterobacter species (3%), Proteus mirabilis (2%), Serratia marcescens (0.6%), and
16 (4.4%), Stenotrophomonas maltophilia (4.3%), Proteus mirabilis (4.0%), Klebsiella oxytoca (2.7%), and
17 lla oxytoca (3), Klebsiella pneumoniae (29), Proteus mirabilis (9), Pseudomonas aeruginosa (10), and
21 Recently, we identified a genomic island of Proteus mirabilis, a common agent of catheter-associated
30 have shown previously using hyperflagellated Proteus mirabilis and a motile but non-swarming flgN tra
31 significant, especially against the bacteria Proteus mirabilis and Antibiotic resistant Escherichia c
33 of Gram-negative bacterial cells, including Proteus mirabilis and Caulobacter crescentus, initiates
36 nodes in these mice isolated K. pneumoniae, Proteus mirabilis and Enterococcus gallinarum, which wer
37 of a urease-negative mutant of uropathogenic Proteus mirabilis and its wild-type parent strain was as
38 during UTI caused by the major uropathogens Proteus mirabilis and Klebsiella pneumoniae, in addition
39 ding Escherichia coli, Providencia stuartii, Proteus mirabilis and Morganella morganii) are shared in
40 operon as a major assimilatory checkpoint in Proteus mirabilis and other Gram-negative bacteria and e
43 zation by urease-positive organisms, such as Proteus mirabilis and Providencia stuartii, commonly occ
44 lebsiella oxytoca, Klebsiella pneumoniae, or Proteus mirabilis and receiving PDAT on blood culture co
45 s II promoter sequences of Escherichia coli, Proteus mirabilis and Salmonella typhimurium allowed det
46 cherichia coli, Pseudomonas aeruginosa PAO1, Proteus mirabilis and Serratia marcescens, possibly by i
47 segregate from other human pathogens such as Proteus mirabilis and Staphylococcus aureus that outcomp
48 coccus faecalis, Pseudomonas aeruginosa, and Proteus mirabilis) and subpopulations of each created by
49 ram-negative pathogens (Escherichia coli and Proteus mirabilis) and variable antifungal activity agai
50 ier studies, lrp genes from Vibrio cholerae, Proteus mirabilis, and E. coli were introduced into the
51 al species including Listeria monocytogenes, Proteus mirabilis, and Escherichia coli in various host
52 ct on the numbers of Salmonella typhimurium, Proteus mirabilis, and Escherichia coli internalized by
55 as Klebsiella pneumoniae, Escherichia coli, Proteus mirabilis, and Salmonella enterica serovar Typhi
56 olates of Escherichia coli, Klebsiella spp., Proteus mirabilis, and Salmonella spp. and are associate
57 by susceptible isolates of Escherichia coli, Proteus mirabilis, and Staphylococcus saprophyticus.
58 ted urinary tract infections (UTI) caused by Proteus mirabilis are associated with severe pathology i
61 ol for application of the mini-Tn7 system in Proteus mirabilis as an example of a bacterium with a se
63 lebsiella pneumoniae, Klebsiella oxytoca, or Proteus mirabilis at >=50 000 colony-forming units/mL; (
64 coli, Klebsiella pneumoniae, K. oxytoca, or Proteus mirabilis at >=50,000 CFU/mL, (2) identification
68 lebsiella pneumoniae, Klebsiella oxytoca, or Proteus mirabilis BSI from a urinary source from May 201
69 Klebsiella pneumoniae, Escherichia coli, and Proteus mirabilis by acidifying the proximal colon and t
73 fundamental behaviors of motile, rod-shaped Proteus mirabilis cells (3 mum in length) adsorbed to th
74 unds on the inhibition of ureolysis in whole Proteus mirabilis cells showed a very good potency (IC(5
75 re also found in cell-free supernatants from Proteus mirabilis, Citrobacter freundii and Enterobacter
80 n CFT073, is a functional homolog of MrpJ of Proteus mirabilis; ectopic expression of papX in P. mira
81 bacterial pathogens: Pseudomonas aeruginosa, Proteus mirabilis, Enterococcus faecalis, Klebsiella pne
82 ns), Listeria monocytogenes (three strains), Proteus mirabilis, Escherichia coli (three strains), and
83 safety, three hazardous foodborne pathogens (Proteus mirabilis, Escherichia coli, and Clostridium bot
84 ted EA rates of >=80%, with the exception of Proteus mirabilis, for which clinical and challenge isol
87 Klebsiella pneumoniae, Escherichia coli, and Proteus mirabilis from the intestinal lumen and represen
90 rming motility by the urinary tract pathogen Proteus mirabilis has been a long-studied but little und
91 -ray crystal structure of a Crl homolog from Proteus mirabilis in conjunction with in vivo and in vit
92 n of inflammatory microbes P. aeruginosa and Proteus mirabilis in ear samples as well as intestinal P
94 se-resistant Proteus-like (MR/P) fimbriae of Proteus mirabilis, indicate that MrpB functions as the t
95 acteriaceae and in particular the pathobiont Proteus mirabilis, induced robust IL-1beta release that
96 , Seo et al. (2015) show that the pathobiont Proteus mirabilis induces NLRP3 inflammasome-dependent i
97 hat provides a clear visual early warning of Proteus mirabilis infection and subsequent blockage.
117 rotease, ZapA, of the urinary tract pathogen Proteus mirabilis is co-ordinately expressed along with
119 loacae isolates, 2 S. marcescens isolates, 1 Proteus mirabilis isolate, and 2 A. baumannii isolates)
121 6 (3%) Klebsiella sp. isolates, and 7 (100%) Proteus mirabilis isolates tested were CTX-M positive, w
122 ebsiella pneumoniae, Klebsiella oxytoca, and Proteus mirabilis isolates, including phenotypically ESB
123 ssified as Corynebacterium frankenforstense, Proteus mirabilis, Lactobacillus johnsonii, and Bacteroi
125 lular migration in a non-swarming but motile Proteus mirabilis mutant lacking the FIgN facilitator of
126 ae (n = 4), Pseudomonas aeruginosa (n = 14), Proteus mirabilis (n = 3), Serratia spp. (n = 10), Steno
127 Intestinal colonization with K. pneumoniae, Proteus mirabilis, or Enterobacter cloacae promoted grea
130 kb PAI, designated ICEPm1, that is common to Proteus mirabilis, Providencia stuartii, and Morganella
131 scherichia coli 1021, Klebsiella pneumoniae, Proteus mirabilis, Providencia stuartii, and Pseudomonas
132 ibrary included probes for Escherichia coli, Proteus mirabilis, Pseudomonas aeruginosa, Enterocococcu
133 gram negative bacteria are Escherichia coli, Proteus mirabilis, Pseudomonas aeruginosa, Klebsiella pn
134 respective homopolymers when challenged with Proteus mirabilis, Pseudomonas aeruginosa, Staphylococcu
137 structures of CaiT from Escherichia coli and Proteus mirabilis revealed an inverted five-transmembran
138 prevent colonization by common uropathogens Proteus mirabilis, Staphylococcus aureus and Escherichia
139 ncluded Gram-negative ( Pseudomonas species, Proteus mirabilis, Stenotrophomonas maltophilia ) and Gr
140 atment enriched the relative proportion of a Proteus mirabilis strain in the ceca of animals not pre-
141 y used to assess the relatedness of swarming Proteus mirabilis strains, was used to study 15 P. aerug
142 by Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Streptococcus pyogenes, Bacillus subt
144 een to identify rhomboid-encoding genes from Proteus mirabilis, tatA was identified as a multicopy su
145 metabolic phenotypes of Escherichia coli and Proteus mirabilis that could not be captured from single
147 In laboratory models of colonization by Proteus mirabilis, the sensor signaled encrustation at a
151 We tested the hypothesis that experimental Proteus mirabilis urinary tract infection in mice would
152 truncated form of hemolysin A (HpmA265) from Proteus mirabilis using a series of functional and struc
154 higher than the averages were observed with Proteus mirabilis versus imipenem and with Klebsiella pn
155 e arfA hairpins from Haemophilus influenzae, Proteus mirabilis, Vibrio fischeri, and Pasteurella mult
156 ty in Escherichia coli, Klebsiella spp., and Proteus mirabilis was evaluated, using incidence rates o
157 to virulence in other pathogens, its role in Proteus mirabilis was investigated by constructing a str
159 genesis of urinary tract infection caused by Proteus mirabilis, we constructed a nonmotile, nonswarmi
160 riminating strains of Myxococcus xanthus and Proteus mirabilis, we found the rates of killing between
161 tract pathogens, Pseudomonas aeruginosa and Proteus mirabilis, were made bioluminescent by stable in
163 his group of compounds was also confirmed in Proteus mirabilis whole-cell-based inhibition assays.
164 ebsiella pneumoniae, Klebsiella oxytoca, and Proteus mirabilis with an ertapenem-susceptible extended
165 inducing drugs also triggered DNA release in Proteus mirabilis, with ssDNA again being more abundant
166 plementation studies with hemolysin-negative Proteus mirabilis WPM111 (a HpmA(-) mutant of BA6163) tr