Candida glabata: Difference between revisions

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Candida glabrata
Candida glabrata
Classification:
Classification:

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Candida glabrata Classification: Kingdom- Fungi Class- Saccharomycetes Order- Saccharomycetales Family- Saccharomycetaceae Genus- Candida Species- glabrata Bacterial- Coccus

Description and Significance: Candida glabrata is responsible for fifteen percent of mucosal candidiasis (fungal infections) due to adhesion to epithelial cells. There is a general consensus that C. glabrata has a strong resistance to any type of antifungal therapies. It is an infectious, haploid yeast with no means of reproduction. Previously, C. glabrata was thought to be non-pathogenic previously, but due to immunosuppressive therapy is now one of the top 3 infectious pathogens. Species was originally discovered in 1917.

Structure and Life Cycle: The bacterial morphology of C. glabrata is coccus haploid yeast. It is a gram positive strain and three to five microns in size. There are many biological processes going on within C. glabrata macrophages including: chromatin organization, protection from DNA breakage and golgi transport. These various processes are what make Candida infections so hard to treat. C. glabrata is the second most invasive Candida species. C. glabrata promotes oral colonizing- mucosal infections mostly in the mouth. Urinalysis can show infections in different areas of the body.

Genome: Chromosome length of C. glabrata is 12,157,105 base pairs. Many base pairs are uncharacterized orthologs. The orthologs have cytoplasm and nucleus localization. Orthologs also contain cytoskeleton, protein binding and lipid binding activity. C. glabrata is a heterogeneous species. C. glabrata’s life cycle was originally proposed to be asexual but recent phylogenetic analysis has showed it is more closely related to sexual yeasts.

Ecology and Pathogenesis: Candida glabrata is pathogenic yeast of increasing medical concern. Often times to test for a C. glabrata infection a urinalysis is done- which often takes a couple days to culture via swabbing and streaking. Detecting C. glabrata is recognized by a “biofilm” forming on urinary catheters and dentures. Most frequently C. glabrata will colonize in the gut (epithial cells) to begin infecting and then spread out to various mucosal pockets in the body. Only a few species of Candida live in the human body, glabrata being one of the few. C. glabrata usually feed off of rotten vegetables or dying plants. A comparable form to a human Candida infection would be any type of fungal infection such as athlete’s foot or a yeast infection (vaginal infections are harder to diagnose). Azole is typically used to treat these various fungal infections but C. glabrata has an innate resistance to azole (Sanglard, 1). C. glabrata is especially prevalent in HIV positive patients due to its pathogenicity to mostly affect the urogenital and bloodstream.

Conclusion: In the past 15 years C. glabrata has risen to one of the top 3 pathogenic, fungal infections. Due to immunotherapy many individuals have become susceptible to it and there are very few ways to treat the infection. C. glabrata has many biological processes going on within it that make it so hard to kill off once infected. It infects mucosal areas by binding to epitheial cells of the body leaving either a ruby red looking rash or on infection sites such as the tongue it leaves a thick white coating.

References: Dongari-Baqtzoqloum, Redding. “Candida glabrata: an Emerging Oral Opportunistic Pathogen.” Department of Oral Health and Diagnostic Sciences: University of Connecticut. March, 2007. Falkow, Ghori, Cormack. “An Adhesion of the Yeast Pathogen Candida glabrata Mediating Adherence to Human Epithelial Cells.” Science Magazine. July 1999. Kaur, Gorityala, Rai, Balusu. “Functional Genomic Analysis of Candida glabrata-macrophage Interaction: Role of Chromatin Remodeling in Virulence.” PLoS Pathogin. August 16th, 2012. Kim, Song, Choi, Chin, Lee, Jeong. “Blood Stream Infections by Candida glabrata: a Single-Center Experience.” Korean J Intern Med. September, 2009. Sanglard. “Loss of Mitochondrial Functions Associated with Azole Resistance in Candida glabrata Results in Enhanced Virulence in Mice.”. Antimicrobial Agents and Chemotherapy. Volume 55, May 2011. Sobel, Vazquez, Fidel. “Candida glabrata: review of epidemiology, pathogenesis and clinical disease with comparison to C. albicans.”. Louisiana State University Medical Center. Department of Microbiology, Immunology and Parasitology, January 12th, 1999. October 6th, 2013.