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    Anticandidal Agents
    Anticandidal Agents
    Anticandidal Agents
    Ebook170 pages1 hour

    Anticandidal Agents

    By Awanish Kumar

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    About this ebook

    Anticandidal Agents provides the latest information on candida drug resistance and its remedial implications. In this compilation, users will find a comprehensive view on overcoming resistance in anticandidal drugs, along with information on novel molecules.

    Candida albicans is an opportunistic pathogenic fungus responsible for life threating invasive and nosocomial infections across the globe. Candidiasis is a major cause of morbidity among immunocompromised patients. Infections caused by non-albicans candida like C. glabrata, C. parapsilosis, and C. tropicalis have also imposed a serious threat in the last few decades. Current treatment of candidiasis relies primarily on antifungal agents broadly categorized as azoles, polyenes, echinocandins, allylamines, and pyrimidines.

    Lately, antifungal resistance has emerged to be an obstruction of current treatment regime. A number of reasons are described in detail. Understanding the mechanisms of resistance is crucial for developing strategies for overcoming the hindrance in current therapeutics.

    • Presents a complete understanding of candida resistance to help in the development of therapeutic expansion and novel drugs
    • Provides thorough information on candida drug resistance and its remedial implications
    • Covers crucial mechanisms of resistance that will help develop strategies for overcoming the hindrance in current therapeutics
    LanguageEnglish
    PublisherAcademic Press
    Release dateSep 12, 2016
    ISBN9780128113127
    Anticandidal Agents
    Author

    Awanish Kumar

    Dr. Awanish Kumar is currently an Associate Professor in the Department of Biotechnology at the National Institute of Technology, Raipur (CG), India. He is working in the area of infection biology, drug targeting, and drug discovery. He has more than 13 years of research experience. He received his PhD in molecular parasitology from the CSIR-Central Drug Research Institute-Lucknow, India and Jawaharlal Nehru University-Delhi, India. He did his post-doctoral study at McGill University, Montreal, Canada. Dr. Kumar has served various national and international organizations in different academic and research capacities. He has authored several monographs, books, and book chapters. He has served on many national committees, scientific society and advisory panels, is a member of many international professional research societies and as a reviewer and editorial board member of reputed and refereed journals.

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      Book preview

      Anticandidal Agents - Awanish Kumar

      Chapter 1

      Introduction

      Abstract

      This chapter of the book includes introductory details of fungal pathogen Candida albicans. We have included the facts of pathogenicity mechanisms like filamentation, white-opaque switching, and biofilm formation. Other characteristics of Candida like genetics and virulence have also been depicted. Brief information of genomic, metabolomic, and proteomic aspects of pathogen has been provided.

      Keywords

      Candida albicans; candidiasis; pathogenicity; virulence

      Candida is a diploid, polymorphic, opportunistic fungus which can exist in yeast, pseudohyphal and hyphal form and is the most common cause of opportunistic mycoses worldwide [1]. Candida are thin-walled, small yeasts (4–6 µm) that can reproduce by budding. There are around 154 species of Candida. Of these, Candida albicans is the most pathogenic species for man that causes candidosis, followed by C. tropicalis, C. stellatoidea, C. glabrata, C. krusei, C. parapsilosis, C. guilliermondii, C. viswanathii, and C. lusitaniae in probable descending order of virulence. Importantly, there has been a recent increase in infections due to non-albicans Candida such as C. glabrata and C. krusei. C. albicans causes almost 100% cases of oropharyngeal candidiasis and at least 90% of cases of Candida vulvovaginitis [2].

      Its growth mode is determined by environmental conditions, i.e., high temperature, high ratio of CO2 to O2, serum, nutrient-poor media, etc. [3]. Usually C. albicans is endogenous in humans and forms part of the normal commensal flora of the oral cavity, large intestine, and vagina. C. albicans is acquired during early postnatal period and remains associated with the human host throughout life. But it becomes pathogenic when the immune functions are impaired resulting in candidiasis which is followed by expansion of the fungus with increased frequency by dissemination via blood stream and colonization of internal organs [4]. This mode of pathogenesis requires the ability to occupy diverse niches of the host and adapt to the changing and adverse conditions present there including that of the host defenses. In order to do so, C. albicans has to express a number of phenotypic properties also called virulent factors like yeast-hyphal transition, white-opaque switching, etc. Candidiasis has become the leading fungal infection in the immunosuppressed population. The mortality rates for systemic infection by Candida ranges from 50% to 100%. Candidiasis is major cause of morbidity among HIV+ patients, intensive care unit patients, and those undergoing cancer chemotherapy or organ transplants. A number of antifungals have been used to treat Candidiasis [5].

      Pathogenesis and Virulence

      The capability of C. albicans to infect such varied host niches is supported by a wide array of virulence factors and fitness attributes. C. albicans is a polymorphic fungus that can grow either as budding yeast, as elongated pseudohyphae, or as true hyphae. Further morphologies include white and opaque cells, formed during switching, and chlamydospores, which are thick-walled spore-like structures. While yeast and true hyphae are regularly observed during infection and have distinct functions (as discussed below), the role of pseudohyphae and switching in vivo is rather unclear and chlamydospores have not been observed in patient samples. Phenotypic plasticity (switching) has been proposed to influence antigenicity and biofilm formation of C. albicans. Yeast cells adhere to host cell surfaces by the expression of adhesins. Contact to host cells triggers the yeast-to-hypha transition. The expression of invasins mediates uptake of the fungus by the host cell through induced endocytosis. The fungus expresses specialized proteins on the cell surface (invasins) that mediate binding to host ligands thereby triggering engulfment of the fungal cell into the host cell. Als3 and Ssa1 bind to host E-cadherin and likely induce endocytosis by a clathrin-dependent

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