Candia albicans is a commensal organism present within the human microbiota that can develop into an opportunistic pathogen. There exists a limited number of antifungal drugs capable of treating severe and invasive infections that can be caused by fungi like C. albicans. Since C. albicans is responsible for many fungal infections, attaining a clear scientific understanding of inhibiting this organism and other fungal species is of vital importance. The primary objective of this research is to map the mechanisms of genetic inhibition within C. albicans which decreases its ability to attach to other microorganisms and potentially decrease C. albicans pathogenicity and proliferation. Additionally, it will demonstrate how other microorganisms like Alcaligenes viscolactis can be used to study attachment mechanisms. Screening a transposon insertion library of Alcaligenes strains, we have identified a pool of mutants that haver reduced binding to C. albicans. The methods used to study the interactions of C. albicans and A. viscolactis include Gram-staining of co-cultures and enumerating the cellular effects of planktonic co-cultures on dilution plates of both microorganisms. Gram stains of these cultures combined with enumeration of colony forming units revealed less proliferation of C. albicans when grown with A. viscolactis than the C. albicans control culture. Multiple bacteria contacting a single yeast cell or its hyphae inhibited the production of more yeast cells within liquid media. These results taken together, indicates a potential inhibition by Alcaligenes against Candida and could potentially identify targets to reduce C. albicans pathogenicity
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