Acute infection of mice with highly virulent group B streptococci as a host resistance model for immunotoxicity assessment

1992 ◽  
Vol 66 (6) ◽  
pp. 423-429 ◽  
Author(s):  
Donna B. Barnes ◽  
J. Michael Hardin ◽  
Stephen B. Pruett
Microbiology ◽  
2006 ◽  
Vol 152 (4) ◽  
pp. 1029-1040 ◽  
Author(s):  
Kyle N. Seifert ◽  
Elisabeth E. Adderson ◽  
April A. Whiting ◽  
John F. Bohnsack ◽  
Paula J. Crowley ◽  
...  

Group B streptococci (GBS) are pathogens of both neonates and adults, with serotype III strains in particular being associated with invasive disease and meningitis. In this study, a novel GBS surface antigen, ε, was found to be co-expressed with the previously reported δ antigen on an identical subset of serotype III GBS. Expression of δ/ε on the surface of serotype III GBS was shown to distinguish the restriction digest pattern (RDP) III-3 and multilocus sequence typing (ST)-17 lineage. ε-Specific antibodies were reactive with a unique, high-molecular-mass, serine-rich repeat protein (Srr-2) found exclusively in RDP III-3 strains. The gene encoding Srr-2 was located within a putative accessory secretory locus that included secY2 and secA2 homologues and had a genetic organization similar to that of the secY2/A2 locus of staphylococci. In contrast, serotype III δ/ε-negative strains and strains representative of serotypes Ia, Ib, Ic and II shared a common Srr-encoding gene, srr-1, and an organization of the secY2/A2 locus similar to that of previously reported serotype Ic, δ/ε-negative serotype III and serotype V GBS strains. Representative serotype III δ/ε-positive strains had LD90 values 3–4 logs less than those of serotype III δ/ε-negative strains in a neonatal mouse model of infection. These results indicate that the RDP III-3/ST-17 lineage expresses Srr-2 and is highly virulent in an in vivo model of neonatal sepsis.


2006 ◽  
Vol 8 (7) ◽  
pp. 1714-1722 ◽  
Author(s):  
Marie-Cécile Lamy ◽  
Shaynoor Dramsi ◽  
Annick Billoët ◽  
Hélène Réglier-Poupet ◽  
Asmaa Tazi ◽  
...  

2011 ◽  
Vol 86 (2) ◽  
pp. 262-265 ◽  
Author(s):  
Marie-Frédérique Lartigue ◽  
Markus Kostrzewa ◽  
Mazen Salloum ◽  
Eve Haguenoer ◽  
Geneviève Héry-Arnaud ◽  
...  

mBio ◽  
2010 ◽  
Vol 1 (3) ◽  
Author(s):  
Uffe B. Skov Sørensen ◽  
Knud Poulsen ◽  
Claudia Ghezzo ◽  
Immaculada Margarit ◽  
Mogens Kilian

ABSTRACTTo examine the global diversity ofStreptococcus agalactiae(group B streptococci [GBS]) and to elucidate the evolutionary processes that determine its population genetics structure and the reported changes in host tropism and infection epidemiology, we examined a collection of 238 bovine and human isolates from nine countries on five continents. Phylogenetic analysis based on the sequences of 15 housekeeping genes combined with patterns of virulence-associated traits identified a genetically heterogeneous core population from which virulent lineages occasionally emerge as a result of recombination affecting major segments of the genome. Such lineages, like clonal complex 17 (CC17) and two distinct clusters of CC23, are exclusively adapted to either humans or cattle and successfully spread globally. The recent emergence and expansion of the human-associated and highly virulent sequence type 17 (ST17) could conceivably account, in part, for the increased prevalence of neonatal GBS infections after 1960. The composite structure of theS. agalactiaegenome invalidates phylogenetic inferences exclusively based on multilocus sequence typing (MLST) data and thereby the previously reported conclusion that the human-associated CC17 emerged from the bovine-associated CC67.IMPORTANCEGroup B streptococci (GBS) (Streptococcus agalactiae) have long been recognized as important causes of mastitis in cattle. After 1960, GBS also became the most prevalent cause of invasive and often fatal infections in newborns. At the same time, GBS are carried by a substantial proportion of healthy individuals. The aims of this study were to elucidate the genetic mechanisms that lead to diversification of the GBS population and to examine the relationship between virulence and host preference of evolutionary lineages of GBS. Genetic analysis of GBS isolates from worldwide sources demonstrated epidemic clones adapted specifically to either the human or bovine host. Such clones seem to emerge from a genetically heterogeneous core population as a result of recombination affecting major segments of the genome. Emergence and global spread of certain clones explain, in part, the change in epidemiology of GBS disease and may have implications for prevention.


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.


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