scholarly journals Epidemiology of Invasive Group B Streptococcal Disease in Alberta, Canada, from 2003 to 2013

2016 ◽  
Vol 54 (7) ◽  
pp. 1774-1781 ◽  
Author(s):  
Areej Alhhazmi ◽  
Donna Hurteau ◽  
Gregory J. Tyrrell
Keyword(s):  
Capsular Polysaccharide ◽  
Late Onset ◽  
Disease Incidence ◽  
Invasive Disease ◽  
Erythromycin Resistance ◽  
Surveillance Period ◽  
Group B Streptococci ◽  
Screening Programs ◽  
Live Births ◽  
Group B

Group B streptococci (GBS) cause severe invasive disease in both neonates and adults. Understanding the epidemiology of GBS provides information that can include determining disease prevalence rates in defined populations and geographic regions, documenting the success of GBS screening programs, and understanding antimicrobial susceptibility patterns. In Alberta, only neonatal invasive GBS (iGBS) disease is notifiable to health authorities. We performed a surveillance study of iGBS in Alberta, Canada, from 2003 to 2013. Over the 11-year period, the disease incidence rate increased from a low of 3.92 cases/100,000 population to a high of 5.99 cases/100,000 population. The capsular polysaccharide serotypes (CPSs) found were CPS III (20.3%), CPS V (19.1%), CPS Ia (18.9%), CPS Ib (12.7%), CPS II (11.1%), CPS IV (6.3%), and nontypeable GBS (9.4%). Rates of early-onset disease (0 to 7 days) increased from 0.15 cases/1,000 live births (in 2003) to 0.34 cases/1,000 live births (in 2013). Rates of late-onset disease (>7 to 90 days) also rose, from 0.15 cases/1,000 live births (in 2003) to 0.39 cases/1,000 live births (in 2013). Alberta also experienced an increase in CPS IV isolates, from 2 cases (in 2003) to 24 cases (in 2013), of which the majority werehvgApositive (86.6%). The predominant sequence type (ST) in 2013 was ST459. Erythromycin resistance rose from 23.6% to 43.9% (in 2013). Clindamycin resistance also increased, from 12.2% to 32.5%. In summary, Alberta, Canada, has experienced an increase in GBS disease; the increase includes both neonatal and adult disease. CPS IV cases also notably increased during the surveillance period, as did resistance to erythromycin and clindamycin.

scholarly journals Trends in molecular characteristics and antimicrobial resistance of group B streptococci: a multicenter study in Serbia, 2015–2020

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Dusan Kekic ◽  
Ina Gajic ◽  
Natasa Opavski ◽  
Milan Kojic ◽  
Goran Vukotic ◽  
...  
Keyword(s):  
Antimicrobial Resistance ◽  
Late Onset ◽  
Group B Streptococcus ◽  
Neonatal Morbidity ◽  
Disease Rate ◽  
Molecular Characteristics ◽  
Group B Streptococci ◽  
Live Births ◽  
Invasive Infections ◽  
Group B

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.

scholarly journals Temporal population structure of invasive Group BStreptococcusduring a period of rising disease incidence shows expansion of a CC17 clone

2018 ◽  
Author(s):  
Dorota Jamrozy ◽  
Marcus C de Goffau ◽  
Merijn W Bijlsma ◽  
Diederik van de Beek ◽  
Taco W. Kuijpers ◽  
...  
Keyword(s):  
Population Structure ◽  
The Netherlands ◽  
Genome Sequencing ◽  
Late Onset ◽  
Disease Incidence ◽  
Invasive Disease ◽  
Whole Genome ◽  
Adhesion Protein ◽  
Group B

AbstractGroup BStreptococcus(GBS) is a major cause of neonatal invasive disease worldwide. In the Netherlands, the incidence of the disease increased, despite the introduction of prevention guidelines in 1999. This was accompanied by changes in pathogen genotype distribution, with a significant increase in the prevalence of isolates belonging to clonal complex (CC) 17. To better understand the mechanisms of temporal changes in the epidemiology of GBS genotypes that correlated with the rise in disease incidence, we applied whole genome sequencing (WGS) to study a national collection of invasive GBS isolates. A total of 1345 isolates from patients aged 0 – 89 days and collected between 1987 and 2016 in the Netherlands were sequenced and characterised. The GBS population contained 5 major lineages representing CC17 (39%), CC19 (25%), CC23 (18%), CC10 (9%), and CC1 (7%). There was a significant rise in the prevalence of isolates representing CC17 and CC23 among cases of early-and late-onset disease, due to expansion of discrete sub-lineages. The most prominent was shown by a CC17 sub-lineage, identified here as CC17-1A, which experienced a major clonal expansion at the end of the 1990s. The CC17-1A expansion correlated with the emergence of a novel phage carrying a gene encoding a putative adhesion protein, named here StrP. The first occurrence of this phage (designated phiStag1) within the collection in 1997, was followed by multiple, independent acquisitions by CC17 and parallel clonal expansions of CC17-1A and another cluster, CC17-1B. The CC17-1A clone was identified in external datasets, and represents a globally distributed invasive sub-lineage of CC17. Our work describes how a sudden change in the epidemiology of specific GBS sub-lineages, in particular CC17-1A, correlates with the rise in the disease incidence, and indicates a putative key role of a novel phage in driving the expansion of this CC17 clone.Author summaryGroup BStreptococcus(GBS) is a commensal organism of the gastrointestinal and genitourinary tracts. However, it is also an opportunistic pathogen and a major cause of neonatal invasive disease, which can be classified into early-onset (0 – 6 days of life) or late-onset (7 – 89 days of life). Current disease prevention strategy involves intrapartum antibiotic prophylaxis (IAP), which aims to prevent the transmission of GBS from mother to baby during labour. Many developed countries adapted national IAP guidelines. In the Netherlands, these were introduced in 1999. However, the incidence of GBS disease increased after IAP introduction. In this study we applied whole genome sequencing to characterise a nationwide collection of invasive GBS from cases of neonatal disease that occurred between 1987 and 2016. Analysis of GBS population structure involving phylogenetic partitioning of individual lineages revealed that the rise in disease incidence involved the expansion of specific clusters from two major GBS lineages, CC17 and CC23. Our study provides new insights into the recent evolution of the ‘hypervirulent’ CC17 and describes a rapid expansion of a discrete, pre-existing sub-lineage that occurred after acquisition of a novel phage carrying a putative adhesion protein gene, underscoring the major role of CC17 in neonatal diseases.

scholarly journals L-Ficolin/Mannose-Binding Lectin-Associated Serine Protease Complexes Bind to Group B Streptococci Primarily through N-Acetylneuraminic Acid of Capsular Polysaccharide and Activate the Complement Pathway

2007 ◽  
Vol 76 (1) ◽  
pp. 179-188 ◽  
Author(s):  
Youko Aoyagi ◽  
Elisabeth E. Adderson ◽  
Craig E. Rubens ◽  
John F. Bohnsack ◽  
Jin G. Min ◽  
...  
Keyword(s):  
Serine Protease ◽  
Specific Antibody ◽  
Capsular Polysaccharide ◽  
Mannose Binding Lectin ◽  
Lectin Pathway ◽  
Group B Streptococci ◽  
Acetylneuraminic Acid ◽  
Mannose Binding ◽  
Group B ◽  
Binding Lectin

ABSTRACT Group B streptococci (GBS) are the most common cause of neonatal sepsis and meningitis. Most infants who are colonized with GBS at birth do not develop invasive disease, although many of these uninfected infants lack protective levels of capsular polysaccharide (CPS)-specific antibody. The lectin pathway of complement is a potential mechanism for initiating opsonization of GBS with CPS-specific antibody-deficient serum. In this study, we determined whether mannose-binding lectin (MBL)/MBL-associated serine protease (MASP) complexes and L-ficolin/MASP complexes bind to different strains of GBS to activate the lectin pathway, and we identified the molecules recognized by lectins on the GBS surface. We found that MBL did not bind to any GBS examined, whereas L-ficolin bound to GBS cells of many serotypes. L-ficolin binding to GBS cells correlated with the CPS content in serotypes Ib, III (restriction digestion pattern types III-2 and III-3), and V but not with the group B-specific polysaccharide (GBPS) content or with the lipoteichoic acid (LTA) content. L-ficolin bound to purified CPS and GBPS in a concentration-dependent manner but not to purified LTA. All strains to which L-ficolin/MASP complexes bound consumed C4. When N-acetylneuraminic acid (NeuNAc) was selectively removed from GBS cells by treatment with neuraminidase, the reduction in L-ficolin binding was correlated with the amount of NeuNAc removed. Additionally, L-ficolin was able to bind to wild-type strains but was able to bind only weakly to unencapsulated mutants and a mutant strain in which the CPS lacks NeuNAc. We concluded that L-ficolin/MASP complexes bind to GBS primarily through an interaction with NeuNAc of CPS.

scholarly journals Changes in incidence and etiology of early-onset neonatal infections 1997–2017 – a retrospective cohort study in western Sweden

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Margrét Johansson Gudjónsdóttir ◽  
Anders Elfvin ◽  
Elisabet Hentz ◽  
Ingegerd Adlerberth ◽  
Ingemar Tessin ◽  
...  
Keyword(s):  
Early Onset ◽  
Antimicrobial Prophylaxis ◽  
List Type ◽  
Neonatal Infections ◽  
Group B Streptococci ◽  
Gram Negative ◽  
Live Births ◽  
Extremely Preterm ◽  
Extremely Preterm Infants ◽  
Group B

Abstract Background The objective of the study was to evaluate data on early-onset neonatal invasive infections in western Sweden for the period 1997–2017. To identify changes in incidence, etiology and mortality and compare to previous studies from the same area starting from 1975. Methods Observational epidemiological, retrospective study on infants 0–6 days of age with a positive culture in blood and/or cerebrospinal fluid between 1997 and 2017. A comparison was made of the incidence between 2008 and 2017 compared to 1997–2007. Changes in the incidence of infections due to Group B streptococci, Staphylococcus aureus and aerobic Gram-negative rods were assessed from 1975. Results The total incidence, including both recognized pathogens and commensals as causative agents, was 1.1/1000 live births. The incidence declined from 1.4/1000 LB in 1997–2007 to 0.9/1000 LB in 2008–2017 but the case-fatality rate remained unchanged, (8/119 vs 7/90), at 7%. Among the 209 patients identified during 1997–2017 with sepsis or meningitis the most common organisms were Group B streptococci (40%, 84/209), S. aureus (16%, 33/209) and E. coli (9%, 18/209). The incidence of Group B streptococci infections went from 0.9/1000 live births 1987–1996 to 0.45/1000 live births 1997–2017 and all cases were within 72 h. The proportion of extremely preterm infants (< 28 weeks gestation) rose steadily during the study period but there was no rise in infections due to Gram-negative organisms. The spectrum of cultured organisms changed after 72 h as commensal organisms started to emerge. Conclusion There has been a decrease in the incidence of neonatal early-onset infections compared to previous studies in western Sweden. The incidence of GBS infections was not as low as in other reports. Further studies are needed to assess if screening-based intra partum antimicrobial prophylaxis instead of a risk factor-based approach for identifying candidates for intrapartum antimicrobial prophylaxis would be a better option for this study area. Key notes This study is one of the longest running follow-ups in the world, a follow-up of 43 years of early-onset neonatal infections.The incidence of early-onset GBS infections is higher in Western Sweden compared to other local reports.No difference in the incidence of early-onset GBS depending on the definition of early-onset being within 72 h or 7 days of life.

scholarly journals Neonatal and young infant sepsis by Group B Streptococci and Escherichia coli: a single-center retrospective analysis in Germany—GBS screening implementation gaps and reduction in antibiotic resistance

2020 ◽  
Vol 179 (11) ◽  
pp. 1769-1777
Author(s):  
Maren Doenhardt ◽  
Barbara Seipolt ◽  
Lars Mense ◽  
Jennifer Lucia Winkler ◽  
Alexander Thürmer ◽  
...  
Keyword(s):  
Early Onset ◽  
Late Onset ◽  
Young Infant ◽  
Antibiotic Use ◽  
Group B Streptococci ◽  
E Coli ◽  
Antimicrobial Substances ◽  
Intrapartum Antibiotic ◽  
Group B ◽  
Implementation Gaps

Abstract The last nationwide surveillance study on neonatal and young infant sepsis due to Group B Streptococci (GBS) and Escherichia coli in Germany was conducted between 2009 and 2010. The aim of this study is to provide longitudinal epidemiological data on neonatal and young infant sepsis caused by GBS and E. coli to reevaluate existing data and to inform clinical decision-making. Every positive blood culture for GBS and E. coli within the first 90 days of life that occurred at our center from 2008 until 2018 was identified. The epidemiological, clinical, laboratory, and microbiological data of all affected patients were analyzed through retrospective chart review, along with the pathogen’s antimicrobial susceptibility results. In total, 106 episodes of neonatal sepsis were described; 31% (n = 33) being caused by GBS and 69% (n = 73) by E. coli; 87% of GBS early-onset disease (EOD) cases did not receive intrapartum antibiotic prophylaxis (IAP). Contrary to general trends, the proportion of resistant E. coli isolates decreased for all tested antibiotics over time. Coincidentally, antenatal antibiotic use beyond IAP during that period decreased significantly in our center. Conclusions: (1) Data at our center suggests at least a regional implementation gap in GBS screening and IAP. (2) The decline in the resistance rate of E. coli for all antimicrobial substances might indicate that the reduction of prenatal antibiotics use is beneficial and that neonatal antibiotic stewardship programs should include pregnant women as well. What is Known:• GBS screening and intrapartum antibiotic prophylaxis led to a 32%-reduction in GBS disease in Germany with a 0.75 (92:122) ratio of early-onset disease to late-onset disease in 2009–2010.• Prenatal antibiotic use might increase the risk of E. coli early-onset disease and antibiotic resistances. What is New:• The GBS early-onset disease rates were twice as high as those of late-onset disease, the ratio was 1.75 (21:12) in 2008–2018 at our institution. This suggests that there are at least regional implementation gaps in the antenatal GBS screening in Germany.• We found a decline in E. coli resistance rates over time for all antimicrobial substances. Reduction in use of prenatal antibiotics might be an explanation.

Group B Streptococcus (Streptococcus agalactiae)

2018 ◽  
Author(s):  
Kirsty Le Doare ◽  
Christine E. Jones ◽  
Paul T. Heath
Keyword(s):  
Early Onset ◽  
Late Onset ◽  
Group B Streptococcus ◽  
Significant Risk ◽  
Neonatal Infection ◽  
Significant Risk Factor ◽  
Invasive Disease ◽  
Neurodevelopmental Outcomes ◽  
Intrapartum Antibiotic ◽  
Group B

Group B Streptococcus (GBS) is a leading cause of early neonatal infection and neonatal mortality, with long-term adverse neurodevelopmental outcomes in up to 50% of survivors of GBS meningitis. GBS has a likely underappreciated role in causing preterm birth and stillbirth. GBS colonizes the vagina and gastrointestinal tract of the pregnant woman, and transmission to the infant occurs during or just before delivery. Although the majority of these infants do not develop invasive disease, maternal colonization is a prerequisite for early onset disease (0–6 days of life, most commonly associated with sepsis and respiratory distress) and a significant risk factor for late onset disease (7–89 days of life, most commonly associated with sepsis and meningitis). The introduction of intrapartum antibiotic prophylaxis has resulted in significant declines in the incidence of early onset disease but provides no protection against late onset disease.

Population structure of group B streptococcus from a low-incidence region for invasive neonatal disease

Microbiology ◽  
2005 ◽  
Vol 151 (6) ◽  
pp. 1875-1881 ◽  
Author(s):  
Naiel Bisharat ◽  
Nicola Jones ◽  
Dror Marchaim ◽  
Colin Block ◽  
Rosalind M. Harding ◽  
...  
Keyword(s):  
Population Structure ◽  
Disease Incidence ◽  
Group B Streptococcus ◽  
Invasive Disease ◽  
Multilocus Genotype ◽  
Neonatal Disease ◽  
Strain Collection ◽  
Low Incidence ◽  
Group B ◽  
Sequence Types

The population structure of group B streptococcus (GBS) from a low-incidence region for invasive neonatal disease (Israel) was investigated using multilocus genotype data. The strain collection consisted of isolates from maternal carriage (n=104) and invasive neonatal disease (n=50), resolving into 46 sequence types. The most prevalent sequence types were ST-1 (17·5 %), ST-19 (10·4 %), ST-17 (9·7 %), ST-22 (8·4 %) and ST-23 (6·5 %). Serotype III was the most common, accounting for 29·2 % of the isolates. None of the serotypes was significantly associated with invasive neonatal disease. burst analysis resolved the 46 sequence types into seven lineages (clonal complexes), from which only lineage ST-17, expressing serotype III only, was significantly associated with invasive neonatal disease. Lineage ST-22 expressed mainly serotype II, and was significantly associated with carriage. The distribution of the various sequence types and lineages, and the association of lineage ST-17 with invasive disease, are consistent with the results of analyses from a global GBS isolate collection. These findings could imply that the global variation in disease incidence is independent of the circulating GBS populations, and may be more affected by other risk factors for invasive GBS disease, or by different prevention strategies.

scholarly journals A unique serine-rich repeat protein (Srr-2) and novel surface antigen (ε) associated with a virulent lineage of serotype III Streptococcus agalactiae

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 ◽  
...  
Keyword(s):  
Surface Antigen ◽  
Invasive Disease ◽  
Group B Streptococci ◽  
Gene Encoding ◽  
Repeat Protein ◽  
Encoding Gene ◽  
Group B ◽  
Mouse Model Of Infection ◽  
Highly Virulent

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.

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