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Genomic analysis reveals new Integrative Conjugal Elements and transposons in GBS conferring antimicrobial resistance

ABSTRACT: ICE in GBS conferring AMR

PROVIDER: PRJEB59039 | ENA |

REPOSITORIES: ENA

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Genomic Analysis Reveals New Integrative Conjugal Elements and Transposons in GBS Conferring Antimicrobial Resistance.

Project description:Streptococcus agalactiae or group B streptococcus (GBS) is a leading cause of neonatal sepsis and increasingly found as an invasive pathogen in older patient populations. Beta-lactam antibiotics remain the most effective therapeutic with resistance rarely reported, while the majority of GBS isolates carry the tetracycline resistance gene tet(M) in fixed genomic positions amongst five predominant clonal clades. In the UK, GBS resistance to clindamycin and erythromycin has increased from 3% in 1991 to 11.9% (clindamycin) and 20.2% (erythromycin), as reported in this study. Here, a systematic investigation of antimicrobial resistance genomic content sought to fully characterise the associated mobile genetic elements within phenotypically resistant GBS isolates from 193 invasive and non-invasive infections of UK adult patients collected during 2014 and 2015. Resistance to erythromycin and clindamycin was mediated by erm(A) (16/193, 8.2%), erm(B) (16/193, 8.2%), mef(A)/msr(D) (10/193, 5.1%), lsa(C) (3/193, 1.5%), lnu(C) (1/193, 0.5%), and erm(T) (1/193, 0.5%) genes. The integrative conjugative elements (ICEs) carrying these genes were occasionally found in combination with high gentamicin resistance mediating genes aac(6')-aph(2″), aminoglycoside resistance genes (ant(6-Ia), aph(3'-III), and/or aad(E)), alternative tetracycline resistance genes (tet(O) and tet(S)), and/or chloramphenicol resistance gene cat(Q), mediating resistance to multiple classes of antibiotics. This study provides evidence of the retention of previously reported ICESag37 (n = 4), ICESag236 (n = 2), and ICESpy009 (n = 3), as well as the definition of sixteen novel ICEs and three novel transposons within the GBS lineage, with no evidence of horizontal transfer.

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Project description:GBS infection in the placenta modules host innate inflammatory response

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Project description:The aim of this study was to investigate the response of human brain endothelial cells to bacterial (group B streptococcus, GBS) infection. Results: GBS WT strain infection results in a specific gene induction pattern that is different from the pilA mutant, but not other mutants such as pilB and srr-1. Conclusion: These findings suggest that the GBS PilA protein contributes to gene induction in brain endothelium.

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Project description:Global regulatory roles of the TCS response regulator CovR in GBS serotype 1a A909 Keywords: Strain comparison; global regulation

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ChIP-seq of the response regulator CovR in Group B Streptococcus (GBS)

Project description:We report the characterization of the major regulator of virulence gene expression (CovR) in Group B Streptococcus. The ChIP-seq experiments define the binding of CovR on the chromosome of the BM110 strain, a representative of the hypervirulent GBS lineage responsible of neonatal meningitis. Regulatory evolution of CovR signaling was investigated by comparing ChIP-seq done in parallel in a second GBS clinical isolate (NEM316) not belonging to the hypervirulent lineage.

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A vaginal tract signal detected by the GBS SaeRS system elicits transcriptomic changes and enhances murine colonization.

Project description:Streptococcus agalactiae (Group B Streptococcus, GBS) can colonize the human vaginal tract leading to both superficial and serious infections in adults and neonates. To study bacterial colonization of the reproductive tract in a mammalian system, we employed a murine vaginal carriage model. Using RNASeq, the transcriptome of GBS growing in vivo during vaginal carriage was determined. Over one-quarter of the genes in GBS were found to be differentially regulated during in vivo colonization as compared to laboratory cultures. A two-component system (TCS) homologous to the staphylococcal virulence regulator SaeRS was identified as being up-regulated in vivo. One of the SaeRS targets, pbsP, a proposed GBS vaccine candidate, was shown to be important for colonization of the vaginal tract. A component of vaginal lavage fluid acted as a signal to turn on pbsP expression via SaeRS. These data demonstrate the ability to quantify RNA expression directly from the murine vaginal tract and identify novel genes involved in vaginal colonization by GBS. They also provide more information about the regulation of an important virulence and colonization factor of GBS, pbsP, by the TCS SaeRS.

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