TY - JOUR
T1 - Epidemiology of Plasmid Lineages Mediating the Spread of Extended-Spectrum Beta-Lactamases among Clinical Escherichia coli
AU - Mahmud, Bejan
AU - Wallace, Meghan A.
AU - Reske, Kimberly A.
AU - Alvarado, Kelly
AU - Muenks, Carol E.
AU - Rasmussen, David A.
AU - Burnham, Carey Ann D.
AU - Lanzas, Cristina
AU - Dubberke, Erik R.
AU - Dantas, Gautam
N1 - Funding Information:
This work was supported in part by awards to G.D. through the National Institute of Allergy and Infectious Diseases of the NIH (grant numbers U01AI123394 and R01AI155893); the Agency for Healthcare Research and Quality (grant number R01HS027621); and the Congressionally Directed Medical Research Program of the US Department of Defense (grant number W81XWH1810225). This work was supported in part by an award to C.L. through the Centers for Disease Control and Prevention (grant number U01CK000587).
Publisher Copyright:
© 2022 Mahmud et al.
PY - 2022/9
Y1 - 2022/9
N2 - The prevalence of extended-spectrum beta-lactamases (ESBLs) among clinical isolates of Escherichia coli has been increasing, with this spread driven by ESBL-encoding plasmids. However, the epidemiology of ESBL-disseminating plasmids remains understudied, obscuring the roles of individual plasmid lineages in ESBL spread. To address this, we performed an in-depth genomic investigation of 149 clinical ESBL-like E. coli isolates from a tertiary care hospital. We obtained high-quality assemblies for 446 plasmids, revealing an extensive map of plasmid sharing that crosses time, space, and bacterial sequence type boundaries. Through a sequencebased network, we identified specific plasmid lineages that are responsible for the dissemination of major ESBLs. Notably, we demonstrate that IncF plasmids separate into 2 distinct lineages that are enriched for different ESBLs and occupy distinct host ranges. Our work provides a detailed picture of plasmid-mediated spread of ESBLs, demonstrating the extensive sequence diversity within identified lineages, while highlighting the genetic elements that underlie the persistence of these plasmids within the clinical E. coli population.
AB - The prevalence of extended-spectrum beta-lactamases (ESBLs) among clinical isolates of Escherichia coli has been increasing, with this spread driven by ESBL-encoding plasmids. However, the epidemiology of ESBL-disseminating plasmids remains understudied, obscuring the roles of individual plasmid lineages in ESBL spread. To address this, we performed an in-depth genomic investigation of 149 clinical ESBL-like E. coli isolates from a tertiary care hospital. We obtained high-quality assemblies for 446 plasmids, revealing an extensive map of plasmid sharing that crosses time, space, and bacterial sequence type boundaries. Through a sequencebased network, we identified specific plasmid lineages that are responsible for the dissemination of major ESBLs. Notably, we demonstrate that IncF plasmids separate into 2 distinct lineages that are enriched for different ESBLs and occupy distinct host ranges. Our work provides a detailed picture of plasmid-mediated spread of ESBLs, demonstrating the extensive sequence diversity within identified lineages, while highlighting the genetic elements that underlie the persistence of these plasmids within the clinical E. coli population.
KW - Escherichia coli
KW - beta-lactamases
KW - plasmid-mediated resistance
UR - http://www.scopus.com/inward/record.url?scp=85140958260&partnerID=8YFLogxK
U2 - 10.1128/msystems.00519-22
DO - 10.1128/msystems.00519-22
M3 - Article
C2 - 35993734
AN - SCOPUS:85140958260
SN - 2379-5077
VL - 7
JO - mSystems
JF - mSystems
IS - 5
ER -