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1 etence and survival following infection with group B Streptococcus.
2 cific role for IKKbeta during infection with group B streptococcus.
3 stinguishable clinically from that caused by group B streptococcus.
4 bacteria such as Listeria monocytogenes and group B streptococcus.
5 with a putative peptidoglycan hydrolase from group B streptococcus.
6 ccus aureus, Staphylococcus epidermidis, and group B Streptococcus.
7 hore A23187, nigericin, Candida albicans and Group B Streptococcus.
8 emic infection with the pathogenic bacterium group B Streptococcus.
9 sociated with lower incidence of early-onset group B streptococcus (0.23 per 1000 livebirths [95% CI
11 neumoniae, 1.1; Neisseria meningitidis, 0.6; group B streptococcus, 0.3; Listeria monocytogenes, 0.2;
13 auses (2 influenza; 2 human herpesvirus 6; 2 group B Streptococcus; 2 Streptococcus pneumoniae; 1 HSV
14 itis, the predominant identified causes were group B streptococcus 25% (16-33), Streptococcus pneumon
18 s of murine and human macrophages induced by group B Streptococcus agalactiae (GBS) is likely an impo
21 tent cytokine response of blood monocytes to group B Streptococcus, although monocytes serve as the k
22 n endothelial cells show enhanced binding to group B Streptococcus and are more susceptible to apopto
24 that nonopsonic recognition between type III group B streptococcus and human neutrophils would occur
25 4-kb foreign DNA element that is shared with group B Streptococcus and is present in all serotype M28
28 maternal immunisation strategies to prevent group B streptococcus and respiratory syncytial virus in
29 hat is known about immune protection against group B streptococcus and respiratory syncytial virus, i
30 cell wall fragments from lysates of type III group B Streptococcus and showed that the complexes cont
33 in 87.0% of the women who were positive for group B streptococcus and who delivered at term, but in
35 ons with strains of the sialylated pathogen, group B Streptococcus, and with sialoglycans presented a
39 acrophage (MPhi) receptor in the response to group B Streptococcus, both in bone marrow-derived MPhis
40 monas aeruginosa, Staphylococcus aureus, and group B streptococcus by increasing membrane permeabilit
41 s derived from a wild-type strain of type Ia group B Streptococcus by selectively inactivating each g
44 K1, groups W-135, Y, and C meningococci, and group B Streptococcus capsular polysaccharides modifies
45 capsular serogroup C (MenC) or Gram-positive group B Streptococcus, capsular type III (GBS-III) bacte
47 ated polysaccharides supports a model of the group B Streptococcus cell surface in which the group B
48 ch 31, 2015, that reported the prevalence of group B streptococcus colonisation in pregnant women.
49 untry and regional heterogeneity in maternal group B streptococcus colonisation is unlikely to comple
51 he estimated mean prevalence of rectovaginal group B streptococcus colonisation was 17.9% (95% CI 16.
52 h enrichment culture method for detection of group B streptococcus colonization in pregnant women.
53 xtraction is a suitable method for detecting group B streptococcus colonization in pregnant women.
56 culture method with the Gen-Probe AccuProbe Group B Streptococcus Culture Test (APGB) and the BD Gen
60 to accurately estimate the global burden of group B streptococcus, especially in low-income countrie
62 The exception was Streptococcus agalactiae (group B Streptococcus), for which non-contaminant signal
63 agar plate (SBAP) and AccuProbe detection of group B streptococcus from overnight LIM broth enhanceme
65 e (n=5), or 2) choriodecidual inoculation of Group B Streptococcus (GBS) 1x10(6) colony forming units
66 The sialylated capsular polysaccharide of group B Streptococcus (GBS) also presents terminal Siaal
67 006, cross-reacts with serogrouping kits for group B Streptococcus (GBS) and could be misidentified i
68 defenses against the frequent human pathogen group B Streptococcus (GBS) and other extracellular bact
69 to inhibit growth and biofilm production in Group B Streptococcus (GBS) and Staphylococcus aureus.
70 e of the BBB to the human meningeal pathogen group B Streptococcus (GBS) and the organism's major vir
72 nant monkeys (Macaca nemestrina) with either group B streptococcus (GBS) at 1 x 10(6) CFU (n = 5) or
73 rd most common cause of neonatal death, with Group B Streptococcus (GBS) being the leading bacterial
76 tinguish between the nine known serotypes of group B streptococcus (GBS) by classical antibody-antige
77 G-independent opsonophagocytosis of type III group B Streptococcus (GBS) by peripheral blood leukocyt
79 genitourinary tracts of pregnant women with group B Streptococcus (GBS) can result in vertical trans
92 rea to determine risk factors for late-onset group B streptococcus (GBS) disease (onset of disease or
93 ps in order to minimize the impact of infant group B streptococcus (GBS) disease in the United Kingdo
95 te substantial progress in the prevention of group B Streptococcus (GBS) disease with the introductio
97 ed infants are at increased risk of invasive Group B Streptococcus (GBS) disease; however, the reason
98 rs for Disease Control guidelines to prevent group B Streptococcus (GBS) early-onset sepsis (EOS) has
103 (GM-CSF) gene-targeted mice (GM-/-) cleared group B streptococcus (GBS) from the lungs more slowly t
104 mistry was utilised to covalently ligate the Group B Streptococcus (GBS) GBS67 protein antigen with t
107 nd universal screening of pregnant women for group B streptococcus (GBS) have further changed the epi
108 flight mass spectrometry (MALDI-TOF MS) for group B streptococcus (GBS) identification, we recovered
110 itive predictive values for the detection of group B Streptococcus (GBS) in 206 LIM enrichment broths
144 Gastrointestinal (GI) colonization with group B Streptococcus (GBS) is an important precursor to
156 accharide (CPS) and some surface proteins by group B Streptococcus (GBS) is regulated by growth rate.
169 Maternal rectovaginal colonization with group B Streptococcus (GBS) is the most common pathway f
170 99 nonpregnant adult Maryland residents with group B Streptococcus (GBS) isolated from a normally ste
171 , we studied the population structure of 102 group B Streptococcus (GBS) isolates prospectively sampl
174 nces of the AmpliVue, BD Max, and illumigene group B Streptococcus (GBS) nucleic acid amplification t
175 eceived choriodecidual inoculation of either group B Streptococcus (GBS) or saline (n = 5/group).
184 on of the human epithelial cell line A549 by group B streptococcus (GBS) serotype VIII strains were c
186 We investigated the association between group B Streptococcus (GBS) serotype-specific capsular p
188 report that neuD, a gene located within the Group B Streptococcus (GBS) Sia biosynthetic gene cluste
189 dies for molecular and serological typing of group B streptococcus (GBS) strains as part of DEVANI (D
192 ansplacental antibody transfer specific to 8 group B Streptococcus (GBS) surface proteins among 81 HI
195 occus aureus, we found the neonatal pathogen group B Streptococcus (GBS) to be remarkably resistant t
196 of immunoglobulin G (IgG) antibodies against group B streptococcus (GBS) type III polysaccharide (PS)
197 to study maternal transfer of antibody to a group B Streptococcus (GBS) type III polysaccharide-teta
198 level of maternal immunoglobulin (Ig) G anti-group B streptococcus (GBS) type III required to protect
203 acterial polysaccharide exotoxin produced by group B Streptococcus (GBS), also referred to as GBS tox
204 women who are rectovaginally colonized with group B Streptococcus (GBS), but the risk of EOGBS from
205 rate kinase (PGK), present on the surface of group B streptococcus (GBS), has previously been demonst
206 rst comprehensive estimates of the burden of group B Streptococcus (GBS), including invasive disease
209 pathogen Streptococcus agalactiae, known as group B Streptococcus (GBS), is the leading cause of bac
210 marily caused by Escherichia coli (E. coli), Group B Streptococcus (GBS), Listeria monocytogenes, Hae
211 , 7 produced at least 1 stool that contained group B Streptococcus (GBS), Serratia marcescens, or Esc
212 In infants, the mode of acquisition of CC17 group B Streptococcus (GBS), the hypervirulent clone res
214 nducting efficacy trials of vaccines against group B streptococcus (GBS), the licensure of these vacc
215 nital inhabitant and opportunistic pathogen, group B Streptococcus (GBS), when present at the time of
230 es of serotype III Streptococcus agalactiae (group B streptococcus [GBS]) can be divided into three s
233 zed 31 isolates of Streptococcus agalactiae (group B Streptococcus [GBS]) from several geographic loc
238 tal infection with Streptococcus agalactiae (group B Streptococcus [GBS]) is a leading cause of sepsi
239 colonization with Streptococcus agalactiae (Group B Streptococcus [GBS]) is a precursor to chorioamn
243 coli, E. faecalis, Streptococcus agalactiae (group B streptococcus [GBS]), or Streptococcus pyogenes
252 -positive bacteria Streptococcus agalactiae (Group B Streptococcus; GBS) type III (GBSIII) and Strept
254 of the CpsA protein of the zoonotic pathogen group B Streptococcus in capsule production and cell wal
257 ntibodies during the acute phase of invasive group B streptococcus infection in nonpregnant adults ma
258 more protective in a neonatal mouse model of group B Streptococcus infection than a vaccine construct
259 vival and conferred resistance to an in vivo group B streptococcus infection, we show that mice with
260 uggish mice displayed high susceptibility to group B streptococcus infection, with impaired TNF-alpha
262 to the observed increase in dissemination of group B Streptococcus into the brain of Hs2st-deficient
272 & Microbe, Andrade et al. (2016) report that Group B Streptococcus limits type I IFN by expressing a
273 to understand these regional differences in group B streptococcus maternal colonisation and early-on
274 e concern that increasing efforts to prevent group B streptococcus neonatal disease may lead to an in
277 -D-/-) and wild-type mice were infected with group B streptococcus or Haemophilus influenzae by intra
279 a 36.3-kb mobile genetic element of apparent group B Streptococcus origin, termed region of differenc
280 the protective response against the type III group B Streptococcus polysaccharide was comprised withi
282 d use of intrapartum antibiotic prophylaxis, group B streptococcus remains a leading cause of morbidi
283 ss several maternal immunisation initiatives-group B streptococcus, respiratory syncytial virus, pert
284 ment of the [D130A,S512A] mutant of SCP from group B Streptococcus (S. agalactiae, SCPB) revealed SCP
286 eningococcal type C polysaccharide (MCPS) or group B Streptococcus serotype V (GBS-V) were unresponsi
288 ght and obesity increased the risk of EOS by group B Streptococcus, Staphylococcus aureus, and Escher
289 esponses to intact Pn14, isolated PPS14, and Group B Streptococcus (strain COH1-11) expressing capsul
290 In this report, we used a mutant strain of group B Streptococcus (Streptococcus agalactiae) type II
291 mologous gene from Streptococcus agalactiae (Group B Streptococcus), Streptococcus equi subsp. zooepi
292 F upon stimulation with Escherichia coli and group B Streptococcus, the leading pathogens of early-on
293 ning of pregnant women for colonization with group B streptococcus to identify candidates for intrapa
295 n antiangiogenic polysaccharide derived from group B streptococcus, was administered by i.v. injectio
296 ed in the cytokine responses to infection by group B Streptococcus We focused on elucidating the func
299 g cause of community-acquired pneumonia, and group B Streptococcus, which causes neonatal sepsis and
300 c.), a selective and differential medium for group B streptococcus, with culture using neomycin-nalid