Biofilm formation and invasive ability contribute to CC17 serotype III group B Streptococcus virulence

AbstractThe hypervirulent Group B Streptococcus (Streptococcus agalactiae, GBS) serogroup III clonal cluster 17 has been associated with neonatal GBS invasive disease and meningits. Serogroup III, ST283 has recently been implicated in invasive disease among non-pregnant adults in Asia. These strains cluster with strains from freshwater fishes from aquaculture and a foodborne outbreak of sepsis, especially with septic arthritis, had been linked to such consumption in Singapore in 2015. Through comparative genome analyses of invasive and non-invasive strains of ST283, we identified a truncated response regulator gene in the non-invasive strain. This two component response gene, previously named a DNA binding regulator, is conserved among GBS strains and is a homologue ofBacillus subtilis BceR, the response regulator of the BceRSAB system. Loss of function of theBceRresponse gene in the invasive GBS strain demonstrated bacitracin susceptibility inΔBceRmutant with MICs of 256-fold and four-fold reduction in bacitracin and human cathelicin LL-37 compared to wild type and complementation strains. Upregulation ofdltAof wild type strain vsΔBceRmutant was demonstrated (p<0.0001), and was previously shown inStaphylococcus aureusto resist and repel cationic peptides through excess positive charges with D-alanylation of teichoic acids on the cell wall. In addition,ΔBceRmutant was less susceptible under oxidative stress under H2O2stress when compared to wild type strain (p<0.001) and inhibited biofilm formation (p<0.05 andp< 0.0001 for crystal violet staining and cfu counts). TheΔBceRmutant also showed reduced mortality as compared to wild type strain (p<0.01) in a murine infection model. Taken together,BceRSis involved in bacitracin and antimicrobial peptide resistance, survival under oxidative stress, biofilm formation and play an important role in the virulence of GBS.Author SummaryTwo-component systems (TCSs) play an important role in virulence in bacteria, and are involved in detecting environmental changes. AlthoughS. agalactiaewas reported to contain more predicted TCSs thanStreptococcus pneumoniae,few have been studied in detail. In this work, comparative genomic analysis of GBS invasive (hyper-virulent) and non-invasive serotype III-4 strains were performed to determine any gene differences that may account for severity of disease in humans.BceR-likeTCS was selected and suspected to be involved in virulence, and thusBceRwas deleted in a hyper-virulent GBS serotype III-4 strain. We demonstrated that thisBceR-likeTCS is involved in GBS virulence and induced proinflammatory host immune responses. Our study of TCSBceRmay guide further research into the role of other TCSs in GBS pathogenicity, and further explore therapeutic targets for GBS disease.

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Antimicrobial Activities of Alginate and Chitosan Oligosaccharides Against Staphylococcus aureus and Group B Streptococcus

Frontiers in Microbiology ◽

10.3389/fmicb.2021.700605 ◽

2021 ◽

Vol 12 ◽

Author(s):

Mostafa Asadpoor ◽

Georgia-Nefeli Ithakisiou ◽

Jos P. M. van Putten ◽

Roland J. Pieters ◽

Gert Folkerts ◽

...

Keyword(s):

Staphylococcus Aureus ◽

Biofilm Formation ◽

Group B Streptococcus ◽

Treatment Strategies ◽

Antimicrobial Activities ◽

Bacterial Biofilm ◽

Chitosan Oligosaccharides ◽

Alginate Oligosaccharides ◽

Novel Treatment Strategies ◽

Group B

The bacterial pathogens Streptococcus agalactiae (GBS) and Staphylococcus aureus (S. aureus) cause serious infections in humans and animals. The emergence of antibiotic-resistant isolates and bacterial biofilm formation entails the urge of novel treatment strategies. Recently, there is a profound scientific interest in the capabilities of non-digestible oligosaccharides as antimicrobial and anti-biofilm agents as well as adjuvants in antibiotic combination therapies. In this study, we investigated the potential of alginate oligosaccharides (AOS) and chitosan oligosaccharides (COS) as alternative for, or in combination with antibiotic treatment. AOS (2–16%) significantly decreased GBS V growth by determining the minimum inhibitory concentration. Both AOS (8 and 16%) and COS (2–16%) were able to prevent biofilm formation by S. aureus wood 46. A checkerboard biofilm formation assay demonstrated a synergistic effect of COS and clindamycin on the S. aureus biofilm formation, while AOS (2 and 4%) were found to sensitize GBS V to trimethoprim. In conclusion, AOS and COS affect the growth of GBS V and S. aureus wood 46 and can function as anti-biofilm agents. The promising effects of AOS and COS in combination with different antibiotics may offer new opportunities to combat antimicrobial resistance.

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Specific Involvement of Pilus Type 2a in Biofilm Formation in Group B Streptococcus

PLoS ONE ◽

10.1371/journal.pone.0009216 ◽

2010 ◽

Vol 5 (2) ◽

pp. e9216 ◽

Cited By ~ 61

Author(s):

Cira Daniela Rinaudo ◽

Roberto Rosini ◽

Cesira L. Galeotti ◽

Francesco Berti ◽

Francesca Necchi ◽

...

Keyword(s):

Biofilm Formation ◽

Group B Streptococcus ◽

Group B

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Human milk oligosaccharides reduce murine group B Streptococcus vaginal colonization with minimal impact on the vaginal microbiota

10.1101/2021.10.20.465155 ◽

2021 ◽

Author(s):

Marlyd E Mejia ◽

Samantha Ottinger ◽

Alison Vrbanac ◽

Priyanka Babu ◽

Jacob Zulk ◽

...

Keyword(s):

Epithelial Cells ◽

Human Milk ◽

Biofilm Formation ◽

Group B Streptococcus ◽

Human Milk Oligosaccharides ◽

Vaginal Colonization ◽

Vaginal Epithelial Cells ◽

Group B

Group B Streptococcus (GBS) colonizes the vaginal mucosa of a significant percentage of healthy women and is a leading cause of neonatal bacterial infections. Currently, pregnant women are screened in the last month of pregnancy and GBS-positive women are given antibiotics during parturition to prevent bacterial transmission to the neonate. Recently, human milk oligosaccharides (HMOs) isolated from breastmilk were found to inhibit GBS growth and biofilm formation in vitro, and women that make certain HMOs are less likely to be vaginally colonized with GBS. Using in vitro human vaginal epithelial cells and a murine vaginal colonization model, we tested the impact of HMO treatment on GBS burdens and the composition of the endogenous microbiota by 16S rRNA amplicon sequencing. HMO treatment reduced GBS vaginal burdens in vivo with minimal alterations to the vaginal microbiota. HMOs displayed potent inhibitory activity against GBS in vitro, but HMO pretreatment did not alter adherence of GBS or the probiotic Lactobacillus rhamnosus to human vaginal epithelial cells. Additionally, disruption of a putative GBS glycosyltransferase (Δsan_0913) rendered the bacterium largely resistant to HMO inhibition in vitro and in vivo but did not compromise its adherence, colonization, or biofilm formation in the absence of HMOs. We conclude that HMOs are a promising therapeutic bioactive to limit GBS vaginal colonization with minimal impacts on the vaginal microenvironment.

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