<i>Candidiasis</i> and Mechanisms of Antifungal Resistance
<i>Candidiasis</i> can be present as a cutaneous, mucosal or deep-seated organ infection, which is caused by more than 20 types of <i>Candida</i> sp., with <i>C. albicans</i> being the most common. These are pathogenic yeast and are usually present in the normal m...
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MDPI AG
2020-06-01
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author | Somanon Bhattacharya Sutthichai Sae-Tia Bettina C. Fries |
author_facet | Somanon Bhattacharya Sutthichai Sae-Tia Bettina C. Fries |
author_sort | Somanon Bhattacharya |
collection | DOAJ |
description | <i>Candidiasis</i> can be present as a cutaneous, mucosal or deep-seated organ infection, which is caused by more than 20 types of <i>Candida</i> sp., with <i>C. albicans</i> being the most common. These are pathogenic yeast and are usually present in the normal microbiome. High-risk individuals are patients of human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS), organ transplant, and diabetes. During infection, pathogens can adhere to complement receptors and various extracellular matrix proteins in the oral and vaginal cavity. Oral and vaginal <i>Candidiasis</i> results from the overgrowth of <i>Candida</i> sp. in the hosts, causing penetration of the oral and vaginal tissues. Symptoms include white patches in the mouth, tongue, throat, and itchiness or burning of genitalia. Diagnosis involves visual examination, microscopic analysis, or culturing. These infections are treated with a variety of antifungals that target different biosynthetic pathways of the pathogen. For example, echinochandins target cell wall biosynthesis, while allylamines, azoles, and morpholines target ergosterol biosynthesis, and 5-Flucytosine (5FC) targets nucleic acid biosynthesis. Azoles are commonly used in therapeutics, however, because of its fungistatic nature, <i>Candida</i> sp. evolve azole resistance. Besides azoles, <i>Candida</i> sp. also acquire resistance to polyenes, echinochandins, and 5FC. This review discusses, in detail, the drug resistance mechanisms adapted by <i>Candida</i> sp. |
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issn | 2079-6382 |
language | English |
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publishDate | 2020-06-01 |
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series | Antibiotics |
spelling | doaj.art-671e0fc5c11e4e2fb2c20bccf091738e2023-11-20T03:17:58ZengMDPI AGAntibiotics2079-63822020-06-019631210.3390/antibiotics9060312<i>Candidiasis</i> and Mechanisms of Antifungal ResistanceSomanon Bhattacharya0Sutthichai Sae-Tia1Bettina C. Fries2Division of Infectious Diseases, Department of Medicine, Stony Brook University, Stony Brook, New York, NY 11794, USADivision of Infectious Diseases, Department of Medicine, Stony Brook University, Stony Brook, New York, NY 11794, USADivision of Infectious Diseases, Department of Medicine, Stony Brook University, Stony Brook, New York, NY 11794, USA<i>Candidiasis</i> can be present as a cutaneous, mucosal or deep-seated organ infection, which is caused by more than 20 types of <i>Candida</i> sp., with <i>C. albicans</i> being the most common. These are pathogenic yeast and are usually present in the normal microbiome. High-risk individuals are patients of human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS), organ transplant, and diabetes. During infection, pathogens can adhere to complement receptors and various extracellular matrix proteins in the oral and vaginal cavity. Oral and vaginal <i>Candidiasis</i> results from the overgrowth of <i>Candida</i> sp. in the hosts, causing penetration of the oral and vaginal tissues. Symptoms include white patches in the mouth, tongue, throat, and itchiness or burning of genitalia. Diagnosis involves visual examination, microscopic analysis, or culturing. These infections are treated with a variety of antifungals that target different biosynthetic pathways of the pathogen. For example, echinochandins target cell wall biosynthesis, while allylamines, azoles, and morpholines target ergosterol biosynthesis, and 5-Flucytosine (5FC) targets nucleic acid biosynthesis. Azoles are commonly used in therapeutics, however, because of its fungistatic nature, <i>Candida</i> sp. evolve azole resistance. Besides azoles, <i>Candida</i> sp. also acquire resistance to polyenes, echinochandins, and 5FC. This review discusses, in detail, the drug resistance mechanisms adapted by <i>Candida</i> sp.https://www.mdpi.com/2079-6382/9/6/312candidiasisantifungal resistanceazole resistanceefflux pumpergosterol biosynthesisechinochandin resistance |
spellingShingle | Somanon Bhattacharya Sutthichai Sae-Tia Bettina C. Fries <i>Candidiasis</i> and Mechanisms of Antifungal Resistance Antibiotics candidiasis antifungal resistance azole resistance efflux pump ergosterol biosynthesis echinochandin resistance |
title | <i>Candidiasis</i> and Mechanisms of Antifungal Resistance |
title_full | <i>Candidiasis</i> and Mechanisms of Antifungal Resistance |
title_fullStr | <i>Candidiasis</i> and Mechanisms of Antifungal Resistance |
title_full_unstemmed | <i>Candidiasis</i> and Mechanisms of Antifungal Resistance |
title_short | <i>Candidiasis</i> and Mechanisms of Antifungal Resistance |
title_sort | i candidiasis i and mechanisms of antifungal resistance |
topic | candidiasis antifungal resistance azole resistance efflux pump ergosterol biosynthesis echinochandin resistance |
url | https://www.mdpi.com/2079-6382/9/6/312 |
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