Testing if the Natural Antimicrobial Manuka Honey Induces A Viable But Not Culturable Bacterial State
Faculty Mentor
Andrea Castillo PhD
Presentation Type
Poster
Start Date
5-8-2024 9:00 AM
End Date
5-8-2024 10:45 AM
Location
PUB NCR
Primary Discipline of Presentation
Biology
Abstract
Antibiotic resistance among bacteria poses a significant threat to global health. Mechanisms that contribute to antibiotic resistance include genetic mutations, acquisition of resistance genes, and transition to persister and Viable But Not Culturable (VBNC) dormant states. While genetically identical to their non-resistant counterparts, persister and VBNC cells evade the effects of antibiotics through metabolic inactivity. Antibiotics are only effective if their targeted processes, e.g., DNA replication, are occurring. Because environmental stressors, notably antibiotics, can induce bacteria to enter dormant states, there is a need for alternative antimicrobials that minimize or do not induce such states. The antimicrobial Manuka Honey (MH) is effective against a wide range of bacteria, without evidence of resistance development. Its multifaceted antimicrobial mechanisms make it a valuable agent for treating bacterial infections. Our research investigates MHs recalcitrance to antibiotic resistance development by testing the hypothesis that MH induces fewer VBNCs than conventional antibiotics. To investigate this, we treated the bacteria Staphylococcus aureus with minimum inhibitory concentrations of MH or the conventional antibiotic tobramycin and then used the viable plate count (VPC) to identify metabolically active cells and the live/dead (LD) staining method to identify all live cells. The number of VBNC cells equals the LD cells number minus the VPC cell number. For S. aureus, tobramycin treatment induced more VBNC cells than MH treatment. We are currently extending our experiments to the bacterial pathogens, Pseudomonas aeruginosa and Escherichia coli. Results of our experiments will elucidate MH’s impact on bacteria physiology and its effectiveness as an antimicrobial.
Recommended Citation
Baker, Lyric T. and Castillo, Andrea PhD, "Testing if the Natural Antimicrobial Manuka Honey Induces A Viable But Not Culturable Bacterial State" (2024). 2024 Symposium. 4.
https://dc.ewu.edu/srcw_2024/ps_2024/p1_2024/4
Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial-No Derivative Works 4.0 International License.
Testing if the Natural Antimicrobial Manuka Honey Induces A Viable But Not Culturable Bacterial State
PUB NCR
Antibiotic resistance among bacteria poses a significant threat to global health. Mechanisms that contribute to antibiotic resistance include genetic mutations, acquisition of resistance genes, and transition to persister and Viable But Not Culturable (VBNC) dormant states. While genetically identical to their non-resistant counterparts, persister and VBNC cells evade the effects of antibiotics through metabolic inactivity. Antibiotics are only effective if their targeted processes, e.g., DNA replication, are occurring. Because environmental stressors, notably antibiotics, can induce bacteria to enter dormant states, there is a need for alternative antimicrobials that minimize or do not induce such states. The antimicrobial Manuka Honey (MH) is effective against a wide range of bacteria, without evidence of resistance development. Its multifaceted antimicrobial mechanisms make it a valuable agent for treating bacterial infections. Our research investigates MHs recalcitrance to antibiotic resistance development by testing the hypothesis that MH induces fewer VBNCs than conventional antibiotics. To investigate this, we treated the bacteria Staphylococcus aureus with minimum inhibitory concentrations of MH or the conventional antibiotic tobramycin and then used the viable plate count (VPC) to identify metabolically active cells and the live/dead (LD) staining method to identify all live cells. The number of VBNC cells equals the LD cells number minus the VPC cell number. For S. aureus, tobramycin treatment induced more VBNC cells than MH treatment. We are currently extending our experiments to the bacterial pathogens, Pseudomonas aeruginosa and Escherichia coli. Results of our experiments will elucidate MH’s impact on bacteria physiology and its effectiveness as an antimicrobial.
