​Evolution of antimicrobial resistance in Group B streptococcus

Evolution of antimicrobial resistance in Group B streptococcus

7/20/2021

Elita Jauneikaite, PhD, BSc (Hons), MRSB

Elita Jauneikaite, PhD, BSc (Hons)

About Presenter

Dr Elita Jauneikaite is an Advanced Research Fellow at Imperial College London, where she leads research on bacterial pathogenesis, global trends in vaccine- preventable infection and antibiotic resistance using bacterial genomics, bioinformatics and molecular biology techniques. Elita’s research programme concentrates on investigating the global trends of disease-causing Group B Streptococcus (GBS) in humans and animals, with a focus on how GBS evolves over time, GBS transmission trends between different hosts and what are the antimicrobial resistance patterns present in disease and carriage GBS isolates. She is also a Research Lead for NIHR HPRU in HCAI and AMR Priority Pathogens theme, where Elita oversees genomics work on other bacterial pathogens including E. coli, K. pneumoniae, methicillin-susceptible S. aureus, S. argenteus and S. pyogenes.

Elita Jauneikaite

7/20/2021 10:52:40 pm

7/20/2021 10:57:51 pm

Marti Perhach

7/20/2021 11:21:09 pm

So glad to have you present for us again, Dr. Jauneikaite! Thank you for sharing your wealth of knowledge on antimicrobial resistance in GBS for ICGBS 2021!

7/22/2021 12:34:57 pm

Dear Marti, thank you very much - its my pleasure to be able to share my insights and research on GBS at this conference.

Roberta Creti

7/21/2021 07:42:37 am

Thanks a lot for your instructive presentation. I'm wondering if the combined use of gentamycin plus beta lactam as empirical antibiotic therapy for neonatal sepsis is shaping the antibiotc resistance profile of GBS, in particular the acquisition of resistance to high level aminoglycosides

elita jauneikaite

7/22/2021 12:39:04 pm

That is a very good point! I am not too familiar with the details of the treatment for cases of neonatal GBS infections, but that could explain a slowly emerging GBS clones with aminoglycoside resistance. With more molecular (and in general) GBS surveillance studies being reported, I hope soon we will be able to pin point specifics of what forces GBS population to expand their AMR clones.

Group B Strep International

7/21/2021 03:16:31 pm

Thank you so much, Dr. Jauneikaite, for your excellent presentation on your very important work. Do you have any insight as to how the MLST genotype distribution might vary for babies who are stillborn? Or would that more likely match the maternal distribution based on whether the mother was colonized or also had invasive disease?

7/22/2021 01:29:26 pm

Thank you for your question. That is a very important question! unfortunately, at the moment there is no molecular study reported on GBS associated with (or recorded as cause of) stillbirth. During the literature review (Bianchi-Jassir et al, 2020; https://doi.org/10.1016/j.vaccine.2020.08.052) we have found only one report on stillbirths and its was reporting only serotype information. But I agree that it would be valuable to know how the isolates from such cases compare to their mother colonisation or disease GBS isolates, and see if there are specific clones causing this.

James Mcgregor

7/21/2021 06:30:26 pm

Astonishing, critical talk . Thank you what about resistance @ ceph’s, clinda? Amino’s ?… early in the discussion I understood you to mention linkage of Tetracycline resistance with increase in neonatal/ obstetric infection. Please clarify? Was this due to additional virulence factors?Your information will be of great importance in showing the advantages of vaccination over antibiotic approaches. Thank you!’

7/22/2021 02:41:35 pm

Yes, resistance to clindamycin and erythromycin has been also detected in GBS and specific genes such as ermB are conferring such resistance to macrolides. ermB as well is present on mobile genetic element and quite often incorporates itself with tetM transposon. Resistance to cephalosporins has been reported in GBS, but thankfully so far is rare (as well as very low rates of GBS resistance to penicillin). Resistance to beta-lactams are usually due to specific mutations in penicillin-binding-proteins (PBPs) in GBS, so these can arise independently from the potential of GBS to acquire mobile genetic element carrying antimicrobial resistance genes.

Regarding the linkage of emergence of GBS in neonatal infections (first GBS neonatal case was reported around 1960s) is around the time when study by da Cunha et al, 2014 (doi: 10.1038/ncomms5544) has estimated the emergence of tetM-carrying GBS clones into human population. As we do not have many isolates available for genomic analysis from before the 2000s, it is hard to look and compare the isolates before and after the tetM-positive strains to test if there virulence profiles differ - but it would really interesting to do that if we could find more older/historical isolates.

7/21/2021 06:40:15 pm

Thanks for presenting again this year. Early in your talk you linked Tetracycline resistance resistance with onset of gbs disease in newborns . Was this a “gain of function”
associated with virulence factor acquisition? Your great knowledge @ resistance will be of crucial importance in adopting gbs vaccination Vs antibiotic use. What about Ceph’s Clinda , others?

7/22/2021 02:42:48 pm

Thank you - I am very glad to hear that you all found my presentation informative. I hope you enjoyed the rest of the conference!

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