Analysis of Reciprocal Inhibition Between Candida albicans and Opportunistic Pathogens Enterobacter aerogenes and Enterobacter cloacae
Faculty Sponsor’s Department
Health Sciences
Name of Project's Faculty Sponsor
Dr. Sean Fox
Type
Poster: Competitive
Project's Category
Microbiology, Morphology, Pathobiology
Abstract or Artist's Statement
The fungal pathogen Candida albicans and the opportunistic bacterial pathogens Enterobacter aerogenes and Enterobacter cloacae are common sources of human disease. The colonization of proximal anatomical locations by these pathogens suggests that interspecies polymicrobial interactions between Candida albicans and Enterobacter species occur. In order to understand mechanisms of diseases caused by these pathogens and to further the study of disease prevention, analyzation of their combined activities was conducted in this study. Changes in fungal morphology, cellular viability, and colony density were investigated using fungal and bacterial co-cultures. The effects of the Candida secreted quorum sensing molecule farnesol on Enterobacter aerogenes and Enterobacter cloacae was studied to observe changes in Enterobacter viability and colony density. The effects of the presence of Enterobacter species on Candida albicans was studied by observing changes in Candida morphology and colony density. The mutant strain of Candida albicans AlS6-/- was also cultured with Enterobacter to determine if the presence of the ALS6 surface glycoprotein gene affected Candida viability and colony density in the presence of Enterobacter species. Statistically significant decreases were observed in all studied metrics between experimental and control groups. This indicated that the interactions observed between Candida albicans and Enterobacter species represent reciprocal inhibitions of cellular functionalities. As Candida albicans is the primary cause of human fungal infections and Enterobacter species are common causes of opportunistic infections, the study of polymicrobial interactions between Candida and Enterobacter species as conducted in this study is important to furthering efforts of human disease inhibition.
Analysis of Reciprocal Inhibition Between Candida albicans and Opportunistic Pathogens Enterobacter aerogenes and Enterobacter cloacae
The fungal pathogen Candida albicans and the opportunistic bacterial pathogens Enterobacter aerogenes and Enterobacter cloacae are common sources of human disease. The colonization of proximal anatomical locations by these pathogens suggests that interspecies polymicrobial interactions between Candida albicans and Enterobacter species occur. In order to understand mechanisms of diseases caused by these pathogens and to further the study of disease prevention, analyzation of their combined activities was conducted in this study. Changes in fungal morphology, cellular viability, and colony density were investigated using fungal and bacterial co-cultures. The effects of the Candida secreted quorum sensing molecule farnesol on Enterobacter aerogenes and Enterobacter cloacae was studied to observe changes in Enterobacter viability and colony density. The effects of the presence of Enterobacter species on Candida albicans was studied by observing changes in Candida morphology and colony density. The mutant strain of Candida albicans AlS6-/- was also cultured with Enterobacter to determine if the presence of the ALS6 surface glycoprotein gene affected Candida viability and colony density in the presence of Enterobacter species. Statistically significant decreases were observed in all studied metrics between experimental and control groups. This indicated that the interactions observed between Candida albicans and Enterobacter species represent reciprocal inhibitions of cellular functionalities. As Candida albicans is the primary cause of human fungal infections and Enterobacter species are common causes of opportunistic infections, the study of polymicrobial interactions between Candida and Enterobacter species as conducted in this study is important to furthering efforts of human disease inhibition.