Project Title

Does Morphology Matter? The Fungal-Bacterial Inhibitory Interactions of Candida albicans and Alcaligenes faecalis.

Authors' Affiliations

Cory Dillard, Aleigha Spaulding, Christopher Prybilla, and Dr. Sean Fox. Department of Health Sciences, College of Public Health, East Tennessee State University, Johnson City, TN

Location

Ballroom

Start Date

4-5-2018 8:00 AM

End Date

4-5-2018 12:00 PM

Poster Number

39

Name of Project's Faculty Sponsor

Dr. Sean Fox

Faculty Sponsor's Department

Department of Health Sciences

Type

Poster: Competitive

Classification of First Author

Undergraduate Student

Project's Category

Biomedical and Health Sciences

Abstract Text

Bacteria and fungi have acquired the ability to interact and survive in many hostile environments both found in nature, as well as, the human body. Candida albicans, an opportunistic fungal pathogen, causes a variety of infections in immunocompromised or immunosuppressed individuals, but also asymptomatically colonizes 80% of the population within the intestinal tract, oral cavity, as well as, the female genitourinary system. A unique capability of C. albicans is the ability to change its morphology from benign circular yeast form, to oval pseudohyphal form, to cylindrical tissue-penetrating hyphal form. Our laboratory has previously identified a bacterium, Alcaligenes faecalis, which displays inhibitory characteristics towards C. albicans. A review of the literature shows that some bacteria have the ability to inhibit C. albicans, but only when in the hyphal form. We therefore wanted to explore if the morphological state of C. albicans dictated the degree of inhibition A. faecalis is able to exude, or simply “does morphology matter?” To determine this effect, a series of both solid and liquid media experiments were performed using a wild-type (able to convert between morphologies) strain of C. albicans, a mutant strain of C. albicans locked into the yeast morphological state, and a mutant strain of C. ablicans locked into the hyphal morphological state. For solid media experiments, the different strains of C. albicans were made into a lawn on agar plates, A. faecalis was spotted onto the lawns, and, after 24 hours, observed for signs of inhibition. For liquid media experiments, C. albicans strains were inoculated alone or co-cultured with A. faecalis for 24 hours and plated to enumerate colony forming units. Our results indicate that: (1) the morphological state of C. albicans is not a determining factor, which is a unique finding compared to other published reports; (2) Both A. faecalis and the closely related A. viscolactis both inhibit C. albicans showing that this is a shared ability among the Alcaligenes genus. (3) that the ability to inhibit C. albicans is thru some form of contact dependent mechanism, as the cell free supernatant of A. faecalis has no inhibitory action. Currently, the exact mechanism for this interaction is unknown, but could be one of the secretion systems bacteria use for interactions with other microbes. As there are very limited treatments for fungal infections and severe side-effects associated with current antifungals, exploiting these mechanisms are medically relevant to human health as they could potentially lead to novel treatments for problematic human fungal pathogens.

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Apr 5th, 8:00 AM Apr 5th, 12:00 PM

Does Morphology Matter? The Fungal-Bacterial Inhibitory Interactions of Candida albicans and Alcaligenes faecalis.

Ballroom

Bacteria and fungi have acquired the ability to interact and survive in many hostile environments both found in nature, as well as, the human body. Candida albicans, an opportunistic fungal pathogen, causes a variety of infections in immunocompromised or immunosuppressed individuals, but also asymptomatically colonizes 80% of the population within the intestinal tract, oral cavity, as well as, the female genitourinary system. A unique capability of C. albicans is the ability to change its morphology from benign circular yeast form, to oval pseudohyphal form, to cylindrical tissue-penetrating hyphal form. Our laboratory has previously identified a bacterium, Alcaligenes faecalis, which displays inhibitory characteristics towards C. albicans. A review of the literature shows that some bacteria have the ability to inhibit C. albicans, but only when in the hyphal form. We therefore wanted to explore if the morphological state of C. albicans dictated the degree of inhibition A. faecalis is able to exude, or simply “does morphology matter?” To determine this effect, a series of both solid and liquid media experiments were performed using a wild-type (able to convert between morphologies) strain of C. albicans, a mutant strain of C. albicans locked into the yeast morphological state, and a mutant strain of C. ablicans locked into the hyphal morphological state. For solid media experiments, the different strains of C. albicans were made into a lawn on agar plates, A. faecalis was spotted onto the lawns, and, after 24 hours, observed for signs of inhibition. For liquid media experiments, C. albicans strains were inoculated alone or co-cultured with A. faecalis for 24 hours and plated to enumerate colony forming units. Our results indicate that: (1) the morphological state of C. albicans is not a determining factor, which is a unique finding compared to other published reports; (2) Both A. faecalis and the closely related A. viscolactis both inhibit C. albicans showing that this is a shared ability among the Alcaligenes genus. (3) that the ability to inhibit C. albicans is thru some form of contact dependent mechanism, as the cell free supernatant of A. faecalis has no inhibitory action. Currently, the exact mechanism for this interaction is unknown, but could be one of the secretion systems bacteria use for interactions with other microbes. As there are very limited treatments for fungal infections and severe side-effects associated with current antifungals, exploiting these mechanisms are medically relevant to human health as they could potentially lead to novel treatments for problematic human fungal pathogens.