Bacterial Infections and Mycoses Commons^™

Transcriptional Regulation Of Azole Antifungal Resistance And Tolerance In Candida Glabrata, Kelly E. Caudle

Theses and Dissertations (ETD)

Azole antifungal resistance has emerged as a significant problem in the management of infections caused by fungi including Candida species. In recent years, Candida glabrata has become the second most common cause of mucosal and invasive fungal infections in humans second to Candida albicans. Not only are systemic C. glabrata infections characterized by high mortality rates, treatment failures to the azole class of antifungals, the most widely used antifungal for treatment of Candida infections, have been reported. Contributing to this problem, C. glabrata exhibits intrinsic reduced susceptibility to the azole antifungals, and the development of high-level azole resistance …

Transcriptional Regulation Of Azole Antifungal Resistance In Candida Albicans, Teresa T. Liu

Theses and Dissertations (ETD)

Candida albicans is a pathogenic fungi found in the mucosa, gastrointestinal, and urogenital tracts of humans. Oropharyngeal candidiasis (OPC), an opportunistic mucosal infection caused by C. albicans, occurs most frequently in patients infected with human immunodeficiency virus (HIV). OPC is usually treated with azole antifungals, a class of antifungals that target ergosterol biosynthesis, at low doses over long periods of time. This course of treatment allows for the development of azole resistance.

Two major mechanisms of azole resistance exist in C. albicans, the up-regulation of genes encoding efflux pumps and the up-regulation of ERG11, a gene encoding the azole drug …

Biochemical And Immunological Mechanisms Underlying Differential Interaction Of Superantigens With Host Immunogenetic Factors In Streptococcal Sepsis, Mohammed Nooh

Theses and Dissertations (ETD)

Group A streptococci (GAS) are serious human pathogens that can cause a wide array of diseases ranging from pharyngitis to streptococcal toxic shock (STSS), which is caused by excessive cytokines responses triggered by streptococcal superantigens (Strep SAgs). SAgs interact simultaneously with HLA class II molecules on antigen presenting cells (APC) and with the T cell receptor beta chain variable elements (TCR V) and cause excessive stimulation of both cell types and massive release of inflammatory mediators.

The Strep SAgs include the streptococcal pyrogenic exotoxins (Spes), which play a crucial role in the pathogenesis of severe invasive streptococcal diseases, including Strep …