1 143 nonduplicate Enterobacter isolates (
102 E. cloacae complex, 41 E. aerogenes) were tested, includ
2 After E. cloacae immunization, MZ B cells were responsible for
3 es of M. morganii, C. freundii, E. coli,
and E. cloacae).
4 In both control
and E. cloacae colonized pigs, HuNoV infection of enterocyte
5 An outbreak of S. marcescens
and E. cloacae bacteremia in a surgical intensive care unit
6 two case patients yielded S. marcescens
and E. cloacae.
7 cter spp., P. aeruginosa, K. pneumoniae,
and E. cloacae.
8 The bacterial isolate was identified
as E. cloacae using a polyphasic approach that included phe
9 However, in our institution the MIC(90)
for E. cloacae bloodstream isolates is 16 microg/ml.
10 cal reevaluation of cefepime breakpoints
for E. cloacae may be prudent.
11 rogenes isolates and 6.0% of the results
for E. cloacae isolates tested with the Vitek system.
12 f the membrane-bound selenate reductase
from E. cloacae SLD1a-1.
13 pigs, reduced HuNoV shedding was observed
in E. cloacae colonized pigs, characterized by significantl
14 nst several Gram-negative bacteria
including E. cloacae but not against Gram-positive bacteria.
15 bla genes revealed that one-third (15/45)
of E. cloacae bloodstream isolates produced SHV-type extend
16 lution) was achieved in only 76/114 (67%)
of E. cloacae isolates (65 susceptible, 11 resistant).
17 Colonization
of E. cloacae also reduced HuNoV titers in intestinal tissu
18 To test the influences
of E. cloacae on HuNoV infectivity and to determine whether
19 In this study involving clinical isolates
of E. cloacae and E. aerogenes, susceptibility testing meth
20 The beta-lactamase
of E. cloacae GC1, an extended spectrum mutant of the P99 e
21 also effectively blocked adhesion of pili
or E. cloacae, but no effect was observed with nonspecific
22 All but two of the ESBL-
producing E. cloacae isolates, but none of the non-ESBL-producing
23 The adhesion of
radiolabeled E. cloacae to HT-29 cells was concentration and temperat
24 sal population underlies multidrug-
resistant E. cloacae infections within hospitals.
25 systematic collection of multidrug-
resistant E. cloacae isolated between 2001 and 2011 from bloodstre
26 016 and 7 previously determined PB-
resistant E. cloacae isolates from JMI Laboratories.
27 In
summary,
E. cloacae inhibited HuNoV infectivity, and B cells were
28 of H2O2 in the leaves of plants 3h after
the E. cloacae inoculation, according to a mechanism involvi
29 Unlike wild-type (WT) forms, such as
the E. cloacae P99 and Citrobacter freundii enzymes, the ES
30 he vast majority of clinical isolates of
the E. cloacae complex, predominantly in (sub)species that f
31 clinically most prevalent subspecies of
the E. cloacae complex.
32 determinant was highly conserved within
the E. cloacae complex and mediated resistance to up to 600
33 h indicates extensive dissemination of
these E. cloacae clones across the UK and Ireland.
34 methods were generally unreliable with
these E. cloacae isolates.
35 Thus E. cloacae NR is not a good candidate for enzymatic prod
36 of bleb-related endophthalmitis secondary
to E. cloacae infection.
37 ed production of DEX-specific Ab titers
upon E. cloacae rechallenge.
38 Catheter infection
with E. cloacae occurred in 50% of roll plates and 80% of bro
39 in vivo, we colonized gnotobiotic pigs
with E. cloacae and inoculated pigs with 2.74 x 10(4) genome
40 r HuNoV in gnotobiotic pigs, with or
without E. cloacae colonization.