Location
D.P. Culp Center Ballroom
Start Date
4-5-2024 9:00 AM
End Date
4-5-2024 11:30 AM
Poster Number
108
Name of Project's Faculty Sponsor
Sean Fox
Faculty Sponsor's Department
Health Sciences
Competition Type
Competitive
Type
Poster Presentation
Presentation Category
Health
Abstract or Artist's Statement
Drug-resistant pathogens have become an increasingly treacherous matter seen globally across healthcare. It has been estimated by the World Health Organization (WHO) that 4.95 million deaths have been a result of antimicrobial resistance. Amongst the vast microbes that play a role in this silent pandemic, one of the most commonly seen is known as Methicillin Resistant Staphylococcus aureus (MRSA). MRSA has become very challenging to combat and usually requires a heavier-hitting antibiotic to show any effect against it. As a result, the hunt for new forms of treatment to overcome this challenge is at an all-time high. It has been previously observed in our laboratory that a bacterium, Alcaligenes faecalis, has the ability to kill or inhibit species found in the genus of Staphylococcus, Bacillus, and the fungal pathogen, Candida. In the present study, we have examined the polymicrobial interactions between A. faecalis and another bacterium, Bacillus subtilis. A mutant library of A. faecalis was constructed by the transformation of a transposon via electroporation and screened on agar plates lawned with B. subtilis to identify loss-of-function mutants that could no longer inhibit the competing bacteria. One particular mutant was observed to no longer produce a zone of inhibition. The genome was isolated from this mutant, AfΔ, and was sequenced to identify the genetic element interrupted. The result was a mutation found in a gene that codes for 3-isopropylmalate dehydratase, an enzyme linked to the metabolic production of leucine. When co-cultured with B. subtilis, the Alcaligenes mutant was no longer able to inhibit B. subtilis as compared to the Alcaligenes wild-type control. This research will be useful in the further study of A. faecalis’ mechanism of action involved in inhibiting the growth of different competing microbes. Once it is fully understood, this information could lead to the development of new targets for therapeutic treatment of drug-resistant Bacillus, Candida, and Staphylococcus infections.
Polymicrobial Interactions Between Alcaligenes faecalis and Human Opportunistic Pathogens: Bacillus, Candida, Staphylococcus species
D.P. Culp Center Ballroom
Drug-resistant pathogens have become an increasingly treacherous matter seen globally across healthcare. It has been estimated by the World Health Organization (WHO) that 4.95 million deaths have been a result of antimicrobial resistance. Amongst the vast microbes that play a role in this silent pandemic, one of the most commonly seen is known as Methicillin Resistant Staphylococcus aureus (MRSA). MRSA has become very challenging to combat and usually requires a heavier-hitting antibiotic to show any effect against it. As a result, the hunt for new forms of treatment to overcome this challenge is at an all-time high. It has been previously observed in our laboratory that a bacterium, Alcaligenes faecalis, has the ability to kill or inhibit species found in the genus of Staphylococcus, Bacillus, and the fungal pathogen, Candida. In the present study, we have examined the polymicrobial interactions between A. faecalis and another bacterium, Bacillus subtilis. A mutant library of A. faecalis was constructed by the transformation of a transposon via electroporation and screened on agar plates lawned with B. subtilis to identify loss-of-function mutants that could no longer inhibit the competing bacteria. One particular mutant was observed to no longer produce a zone of inhibition. The genome was isolated from this mutant, AfΔ, and was sequenced to identify the genetic element interrupted. The result was a mutation found in a gene that codes for 3-isopropylmalate dehydratase, an enzyme linked to the metabolic production of leucine. When co-cultured with B. subtilis, the Alcaligenes mutant was no longer able to inhibit B. subtilis as compared to the Alcaligenes wild-type control. This research will be useful in the further study of A. faecalis’ mechanism of action involved in inhibiting the growth of different competing microbes. Once it is fully understood, this information could lead to the development of new targets for therapeutic treatment of drug-resistant Bacillus, Candida, and Staphylococcus infections.