SEROTYPE CHARACTERISTICS OF GROUP B STREPTOCOCCI CAUSING INVASIVE INFECTION COMPARED WITH COLONIZING STRAINS ISOLATED FROM JAPANESE INFANTS

Author(s):  
Meiwa Toyofuku
2005 ◽  
Vol 73 (3) ◽  
pp. 1671-1683 ◽  
Author(s):  
Ravin Seepersaud ◽  
Sean B. Hanniffy ◽  
Peter Mayne ◽  
Phil Sizer ◽  
Richard Le Page ◽  
...  

ABSTRACT Group B streptococci (GBS) usually behave as commensal organisms that asymptomatically colonize the gastrointestinal and urogenital tracts of adults. However, GBS are also pathogens and the leading bacterial cause of life-threatening invasive disease in neonates. While the events leading to transmission and disease in neonates remain unclear, GBS carriage and level of colonization in the mother have been shown to be significant risk factors associated with invasive infection. Surface antigens represent ideal vaccine targets for eliciting antibodies that can act as opsonins and/or inhibit colonization and invasion. Using a genetic screen for exported proteins in GBS, we identified a gene, designated lrrG, that encodes a novel LPXTG anchored surface antigen containing leucine-rich repeat (LRR) motifs found in bacterial invasins and other members of the LRR protein family. Southern blotting showed that lrrG was present in all GBS strains tested, representing the nine serotypes, and revealed the presence of an lrrG homologue in Streptococcus pyogenes. Recombinant LrrG protein was shown in vitro to adhere to epithelial cells in a dose-dependent manner, suggesting that it may function as an adhesion factor in GBS. More importantly, immunization with recombinant LrrG elicited a strong immunoglobulin G response in CBA/ca mice and protected against lethal challenge with virulent GBS. The data presented in this report suggest that this conserved protein is a highly promising candidate antigen for use in a GBS vaccine.


Author(s):  
Francesco Coppolino ◽  
Letizia Romeo ◽  
Giampiero Pietrocola ◽  
Germana Lentini ◽  
Giuseppe Valerio De Gaetano ◽  
...  

Binding to plasminogen (Plg) enables bacteria to associate with and invade host tissues. The cell wall protein PbsP significantly contributes to the ability of group B streptococci, a frequent cause of invasive infection, to bind Plg. Here we sought to identify the molecular regions involved in the interactions between Plg and PbsP. The K4 Kringle domain of the Plg molecule was required for binding of Plg to whole PbsP and to a PbsP fragment encompassing a region rich in methionine and lysine (MK-rich domain). These interactions were inhibited by free L-lysine, indicating the involvement of lysine binding sites in the Plg molecule. However, mutation to alanine of all lysine residues in the MK-rich domain did not decrease its ability to bind Plg. Collectively, our data identify a novel bacterial sequence that can interact with lysine binding sites in the Plg molecule. Notably, such binding did not require the presence of lysine or other positively charged amino acids in the bacterial receptor. These data may be useful for developing alternative therapeutic strategies aimed at blocking interactions between group B streptococci and Plg.


1985 ◽  
Vol 17 (2) ◽  
pp. 191-193
Author(s):  
Chris Mulder ◽  
Pieter Bol ◽  
Arjan Nabbe ◽  
Bob Zanen

1999 ◽  
Vol 86 (1) ◽  
pp. 61-65 ◽  
Author(s):  
Richard M. Whitehurst ◽  
Rachel Laskey ◽  
Ronald N. Goldberg ◽  
Donald Herbert ◽  
Cornelius Van Breemen

To study whether a sepsis-induced increase in des-Arg9-bradykinin (des-Arg9-BK) and bradykinin (BK) B1-receptor activity participates in the observed increase in pulmonary vascular resistance in neonatal group B streptococcal sepsis (GBS), isometric force bioassays of pulmonary artery (PA) rings were studied, after 4-h exposure to either Krebs or GBS, by using the following protocols: 1) BK dose-response curve, 2) vascular response to BK with N G-nitro-l-arginine methyl ester (l-NAME), and 3) response to des-Arg9-BK (BK metabolite and B1 agonist). PA rings exposed to BK resulted in contraction in the GBS group and a decrease in resting tension in the Control group ( P = 0.034) at a concentration of 10−5 M. GBS-treated PA rings contracted more to des-Arg9-BK than did Controls ( P < 0.001). BK (10−6 M) relaxed preconstricted PA rings incubated in GBS less than BK relaxed Controls ( P < 0.001), and preincubation withl-NAME decreased relaxation in both. These results suggest that GBS decreased endothelium-dependent BK relaxation and increased contractile response to des-Arg9-BK. We speculate that this occurs secondary to upregulation of B1 receptors reflected by B1-agonist-mediated PA contraction.


1977 ◽  
Vol 2 (15) ◽  
pp. 500-501 ◽  
Author(s):  
Leslie R. Ashdown ◽  
P. H. Hewson ◽  
S. K. Suleman
Keyword(s):  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Dusan Kekic ◽  
Ina Gajic ◽  
Natasa Opavski ◽  
Milan Kojic ◽  
Goran Vukotic ◽  
...  

AbstractGroup B Streptococcus (GBS) is a major cause of neonatal morbidity and mortality. Serbia has not fully implemented preventive measures against GBS neonatal diseases. Therefore, we aimed to assess the maternal GBS colonisation and invasive neonatal disease rate, to reveal the trends of antimicrobial resistance and serotype distribution of GBS from various patient groups. Randomly selected non-invasive (n = 991) and all invasive GBS (n = 80) collected throughout Serbia from 2015 to 2020 were tested for antimicrobial susceptibility, capsular typing, and hvgA detection. Overall, 877/5621 (15.6%) pregnant women were colonised with GBS. Invasive GBS infections incidence in infants (0.18/1000 live births) showed a decreasing trend (0.3 to 0.1/1000 live births). Type III was overrepresented in infants with invasive infections (n = 35, 58.3%), whereas type V predominated among colonised adults (n = 224, 25.5%) and those with noninvasive (n = 37, 32.5%) and invasive infections (n = 8, 40%). The hypervirulent clone III/ST17 was highly associated with invasive infections (n = 28, 35%), particularly late-onset disease (n = 9, 47.4%), showing an increase from 12.3 to 14.8%. The GBS resistance to erythromycin and clindamycin was 26.7% and 22.1%, respectively, with an upward trend. The emergence of the hypervirulent clone III/ST17 and the escalation in GBS resistance highlight an urgent need for continuous monitoring of GBS infections.


1991 ◽  
Vol 163 (4) ◽  
pp. 792-798 ◽  
Author(s):  
H. R. Hill ◽  
L. A. Gonzales ◽  
W. A. Knappe ◽  
G. W. Fischer ◽  
D. K. Kelsey ◽  
...  

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