Loading...
THE ENTEROCOCCUS FAECALIS VIRULENCE PLAMISD pCF10 INDUCES RIGID STRUCTURE FORMATION AND ENHANCES RESISTANCE TO ANTIBIOTIC KILLING
Jean-Baptiste, Herby Charles
Jean-Baptiste, Herby Charles
Citations
Altmetric:
Genre
Thesis/Dissertation
Date
2023-12
Advisor
Committee member
Group
Department
Biomedical Sciences
Subject
Permanent link to this record
Collections
Research Projects
Organizational Units
Journal Issue
DOI
http://dx.doi.org/10.34944/dspace/9487
Abstract
Enterococci are gram-positive cocci commensals found mostly in the gastrointestinal tract of humans and animals. Acquisition of mobile genetic elements increases their pathogenicity and transforms the bacteria into multidrug resistance (MDR) opportunistic pathogens that are the causative agents for UTI, endocarditis, and septicemia infections. When the pheromone responsive plasmid pCF10 was introduced into the commensal type strain OG1 derivatives OG1RF and OG1SSP, the production of densely packed rigid structures in the otherwise viscous OG1RF/OG1SSP biofilms was observed using optical bottom 24-well plate cultures and confocal microscopy. A steady state population of an average of 2 x 108 cells/biofilm was reached within 24 h with fresh media changes twice a day. However, biofilm remodeling continued over 3 days with increasing size of rigid structures. Formation of rigid structures requires aggregation substance (AS), a produced by Enterococci. A similar phenotype of smaller structures with chains is observed in markerless aggregation substance mutants (ΔprgB) and a pCF10 subclone pMSP6050 not containing prgB. Th genes accounting for the chaining phenotype in pMSP6050 are currently under investigation. We noted different structures are affected differently by antibiotics, and treatment of antibiotic killed loosely packed biofilm, but the rigid structures continued to grow depending on their size. The quick remodeling (within 1 hour) and new 1-log higher steady state number of bacteria is hypothesized to be due to protected microenvironments observed in our rigid structures. This new development is primarily the drive and focus of our collaboration with the Queisser Lab (Dept. of Mathematics, Temple Univ.) to develop a computational model that mirrors this behavior described above. In addition to known roles of ordered matrix materials, such as amyloids, our studies suggest that aggregation is sufficient to produce rigid structures, and that the biofilm communities reach steady state with slowing increasing size of the rigid structures. Under antibiotic pressure, there is an observed remodeling and an increase of the steady population in our treated cells suggesting growth in protected microenvironments.
Description
Citation
Citation to related work
Has part
ADA compliance
For Americans with Disabilities Act (ADA) accommodation, including help with reading this content, please contact scholarshare@temple.edu