scholarly journals Mutually Exclusive Distribution of IS1548 and GBSi1, an Active Group II Intron Identified in Human Isolates of Group B Streptococci

2001 ◽  
Vol 183 (8) ◽  
pp. 2560-2569 ◽  
Author(s):  
Margareta Granlund ◽  
François Michel ◽  
Mari Norgren

ABSTRACT The present study shows that active, self-splicing group II intron GBSi1 is located downstream of the C5a-peptidase gene,scpB, in some group B streptococcus (GBS) isolates that lack insertion sequence IS1548. IS1548 was previously reported to be often present at the scpB locus in GBS isolated in association with endocarditis. Since none of 67 GBS isolates examined, 40 of which were of serotype III, harbored both IS1548 and GBSi1, these two elements are suggested to be markers for different genetic lineages in GBS serotype III. The DNA region downstream of scpB in GBS isolates harboring either GBSi1, IS1548, or none of these mobile elements was found to encode the laminin binding protein, Lmb, which shows sequence similarities to a family of streptococcal adhesins. IS1548 is inserted 9 bp upstream of the putative promoter for lmb, while the insertion site for GBSi1 is located 88 bp further upstream. Sequences highly similar to GBSi1 exist also in Streptococcus pneumoniae. An inverted repeat sequence, with features typical of transcription terminators, was identified immediately upstream of the insertion site for the group II intron both in the GBS and S. pneumoniae sequences. This motif is suggested to constitute a target for the GBS intron as well as for rather closely related introns in Bacillus halodurans, Pseudomonas alcaligenes, andPseudomonas putida. When transcripts containing the GBSi1 intron were incubated at high concentrations of ammonium and magnesium, a major product with the expected length and sequence for the ligated exons was generated. Unlike, however, all members of group II investigated so far, the excised intron was in linear, rather than in a branched (lariat), form.

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.


PEDIATRICS ◽  
1977 ◽  
Vol 60 (4) ◽  
pp. 473-476 ◽  
Author(s):  
Margaret R. Hammerschlag ◽  
Carol J. Baker ◽  
Susan Alpert ◽  
Dennis L. Kasper ◽  
Ingrid Rosner ◽  
...  

Cultures from the vagina, pharynx, and anal canal of 100 healthy girls, 2 months through 15 years of age, were examined for the presence of group B streptococci. Of the 100 participants, 20% were colonized at one or more of these three sites. Pharyngeal colonization was detected in 15% of the girls under 11 years of age and in 5% of those over 11 years of age. Colonization at anogenital sites was observed in 19% of participants under 3 years of age, in 25% of those 11 years of age and older, and in only 4% of those between the ages of 3 and 10 years (P < .025). The concentration of serum antibody directed against the polysaccharide capsular antigen isolated from type III, group B Streptococcus appeared, in part, to be related to increasing age.


2003 ◽  
Vol 71 (12) ◽  
pp. 6857-6863 ◽  
Author(s):  
Elisabeth E. Adderson ◽  
Shinji Takahashi ◽  
Yan Wang ◽  
Jianling Armstrong ◽  
Dylan V. Miller ◽  
...  

ABSTRACT Group B Streptococcus agalactiae bacteria (group B streptococci [GBS]) are the most common cause of serious bacterial infection in newborn infants. The majority of serotype III-related cases of neonatal disease are caused by a genetically related subgroup of bacteria, restriction fragment digest pattern (RDP) type III-3, suggesting that these strains possess unique genes contributing to virulence. We used genomic subtractive hybridization to identify regions of genomic DNA unique to virulent RDP type III-3 GBS strains. Within one of these III-3-specific regions is a 1,506-bp open reading frame, spb1 (surface protein of group B streptococcus 1). A mutant type III GBS strain lacking Spb1 was constructed in virulent RDP type III-3 strain 874391, and the interactions of the wild-type and spb1 isogenic mutant with a variety of epithelial cells important to GBS colonization and infection were compared. While adherence of the spb1 isogenic mutant to A549 respiratory, C2Bbe1 colonic, and HeLa cervical epithelial cells was slightly lower than that of the 874391 strain, invasion of the Spb1− mutant was significantly reduced with these cell lines compared to what was seen with 874391. The defect in epithelial invasion was corrected by supplying spb1 in trans. These observations suggest that Spb1 contributes to the pathogenesis of neonatal GBS infection by mediating internalization of virulent serotype III GBS and confirm that understanding of the population structure of bacteria may lead to insights into the pathogenesis of human infections.


2018 ◽  
Vol 67 (5) ◽  
pp. 62-73
Author(s):  
Vasilisa A. Vasilyeva ◽  
Elena V. Shipitsyna ◽  
Kira V. Shalepo ◽  
Alevtina M. Savicheva

Hypothesis/aims of study. The present analysis was undertaken to summarize current knowledge about molecular properties of group B streptococci (GBS), emphasizing potential targets of vaccines against neonatal GBS infection. Study design, materials, and methods. This review is based on articles published mainly in the last ten years. Results. Epidemiological data on serotypes, multilocus sequence types, clonal complexes of GBS and their relationship are presented. Genetic events in GBS populations indicate significant obstacles to vaccine development. We described key properties of major GBS virulence factors, such as capsular polysaccharide, pili, and cell adhesion molecules, as well as results of experimental immunization on their basis. Conclusion. The population of invasive GBS strains is molecularly and genetically heterogeneous, which complicates selection of vaccine targets. Capsular switching, a low level of immunogenicity and variability of population composition are the most important factors that necessitate the accumulation and monitoring of molecular epidemiological data.


PEDIATRICS ◽  
1981 ◽  
Vol 68 (4) ◽  
pp. 544-549 ◽  
Author(s):  
Carol J. Baker ◽  
Morven S. Edwards ◽  
Dennis L. Kasper

The role of maternally acquired antibody to native type III polysacchande of group B Streptococcus as a determinant of susceptibility for infant systemic infection was investigated. Sera from 11 1 acutely ill infants with type III group B streptococcal bacteremia and/or meningitis and their mothers, and cord sera from 45 healthy neonates and their mothers who had type III group B streptococcal vaginal colonization at delivery were studied. Sera from each of 111 acutely ill infants contained very low levels ofantibody (sjlt 1.7 µg/ml, median 0.4 µg/ml), and a significant correlation with maternal levels was tested for early onset infection (median 0.6 µg/ml; r = .76; P sjlt .01). Women whose infants remained well had antibody levels sjgt 2 µg/ml in their sera (73%) more often than those whose infants developed symptomatic infection (17%) (P sjlt .001), and the median level in their sera (12.6 µg/ml) was considerably higher. Study of sera obtained during convalescence from 86 surviving infants indicated a poor antibody response to infection. In contrast, high levels of antibody were detected in sera from each of five convalescent women with postpartum bacteremia. These data extend earlier observations suggesting the correlation between low levels of type-specific antibody in serum and risk for systemic infection with type III strains of group B streptococci.


2005 ◽  
Vol 187 (17) ◽  
pp. 6248-6252 ◽  
Author(s):  
Geneviève Héry-Arnaud ◽  
Guillaume Bruant ◽  
Philippe Lanotte ◽  
Stella Brun ◽  
Agnès Rosenau ◽  
...  

ABSTRACT The prevalence of insertion sequences IS1548, IS861, IS1381, and ISSa4 and of the group II intron GBSi1 within Streptococcus agalactiae human isolates strongly correlates with the genetic lineages obtained by multilocus sequence typing. Our results yielded an evolutionary scheme for the acquisition of these genetic elements linked to the ecosystems from which the isolates were obtained.


1986 ◽  
Vol 7 (S2) ◽  
pp. 135-137 ◽  
Author(s):  
Charles S.F. Easmon

Over the past 25 years group B streptococci have become established as one of the main bacterial pathogens of the neonate in Western Europe and the United States. The attack rate of 0.25/1,000 live births found by Mayon White in Great Britain1 appears typical of many European countries. However, in some centers in the United States attack rates can be over 10 times higher.Two types of neonatal group B streptococcus (GBS) diseases exist, “early” and “late” onset. Early onset disease usually presents within the first few days of life. Often the most serious infections are present at birth or seen within a few hours. Early onset disease presents with pneumonia, respiratory distress and shock. Bacteremia is normally present and meningitis may occur. Mortality is high (50% to 75%). The portal of entry is probably the respiratory tract. Infants normally acquire the infecting organism from their mothers. Heavy maternal and infant colonization, prolonged rupture of membranes, prematurity, and obstetric complications are all risk factors.Delayed onset disease, as its name suggests, presents after the first week of life, primarily with bacteremia and meningitis. Mortality is much lower than for the early onset form, but still appreciable for a bacterial infection (14% to 18%). Its epidemiology is uncertain.


2009 ◽  
Vol 138 (7) ◽  
pp. 979-981 ◽  
Author(s):  
A. DHANOA ◽  
R. KARUNAKARAN ◽  
S. D. PUTHUCHEARY

SUMMARYGroup B streptococcus (GBS) is a leading cause of neonatal sepsis and is usually acquired via the woman's birth canal. GBS serotypes isolated from 200 pregnant women were determined. Serotypes V (19%) and VI (17%) were the most frequent followed by serotypes III (12%), Ia (11·5%) and IV (10%); 17% of the strains were non-typable. All isolates were susceptible to penicillin, 96% to erythromycin and 97·5% to clindamycin. The emergence of new GBS serotypes has important implications for vaccine prevention strategies.


2004 ◽  
Vol 72 (8) ◽  
pp. 4716-4722 ◽  
Author(s):  
Hiroshige Mikamo ◽  
Atul K. Johri ◽  
Lawrence C. Paoletti ◽  
Lawrence C. Madoff ◽  
Andrew B. Onderdonk

ABSTRACT The adherence to and invasion of the human epithelial cell line A549 by group B streptococcus (GBS) serotype VIII strains were compared with those of serotype III strains by a conventional method and the dynamic in vitro attachment and invasion system. Twenty GBS strains, including nine vaginal isolates and one invasive isolate each of serotypes III and VIII, were used in the conventional attachment and invasion assay. Adherence to and invasion of A549 cells by serotype VIII GBS strains were significantly greater (P < 0.0001) than those by serotype III strains for both the invasive strain and vaginal isolates. Cytokine production by A549 cells following stimulation with GBS serotypes III and VIII or their purified capsular polysaccharides (CPS) was measured. Serotype III strains stimulated significantly greater tumor necrosis factor alpha (TNF-α) (P < 0.0001) and interleukin-10 (IL-10) (P < 0.05) production than did serotype VIII strains. IL-8 production in response to serotype VIII was significantly higher (P < 0.001) than that in response to serotype III. TNF-α, IL-8, and IL-10 production was greater in A549 cells infected with GBS than in the untreated control cells. TNF-α production was significantly greater (P < 0.005) after stimulation with purified GBS serotype III CPS than after stimulation with serotype VIII CPS, a result similar to that after stimulation with whole GBS. IL-12 production by A549 cells was observed only in response to infection with GBS serotype III, resulting in the possibility of a greater TH1 response in serotype III GBS. These results suggest differences in immune responses to infection with GBS serotypes III and VIII.


1999 ◽  
Vol 67 (4) ◽  
pp. 1866-1870 ◽  
Author(s):  
Shinji Takahashi ◽  
Youko Aoyagi ◽  
Elisabeth E. Adderson ◽  
Yoshiyuki Okuwaki ◽  
John F. Bohnsack

ABSTRACT The majority of type III group B streptococcus (GBS) human neonatal infections are caused by a genetically related subgroup called III-3. We have proposed that a bacterial enzyme, C5a-ase, contributes to the pathogenesis of neonatal infections with GBS by rapidly inactivating C5a, a potent pro-inflammatory molecule, but many III-3 strains do not express C5a-ase. The amount of C5a produced in serum following incubation with representative type III strains was quantitated in order to better understand the relationship between C5a production and C5a-ase expression. C5a production following incubation of bacteria with serum depleted of antibody to the bacterial surface was inversely proportional to the sialic acid content of the bacterial capsule, with the more heavily sialylated III-3 strains generating less C5a than the less-virulent, less-sialylated III-2 strains. The amount of C5a produced correlated significantly with C3 deposition on each bacterial strain. Repletion with type-specific antibody caused increased C3b deposition and C5a production through alternative pathway activation, but C5a was functionally inactivated by strains that expressed C5a-ase. The increased virulence of III-3 strains compared to that of III-2 strains results at least partially from the higher sialic acid content of III-3 strains, which inhibits both opsonophagocytic killing and C5a production in the absence of type-specific antibody. We propose that C5a-ase is not necessary for III-3 strains to cause invasive disease because the high sialic acid content of III-3 strains inhibits C5a production.


Sign in / Sign up

Export Citation Format

Share Document