Pathogenesis of invasive candidiasis
Autor: | Theodore C. White, N. Agabian, Daniel Poulain, David R. Soll, Frank C. Odds |
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Rok vydání: | 1994 |
Předmět: |
Infectivity
biology Genes Fungal Candidiasis Defence mechanisms Virulence General Medicine Fungus biology.organism_classification medicine.disease Virulence factor Corpus albicans Host-Parasite Interactions Microbiology Mannans Infectious Diseases Candida albicans Immunology medicine Aspartic Acid Endopeptidases Humans Genes Switch Mycosis |
Zdroj: | Europe PubMed Central |
ISSN: | 1460-2709 1369-3786 |
DOI: | 10.1080/02681219480000861 |
Popis: | Candida infection: an overview of the host-parasite relationship Interactions between Candida albicans and its mammalian hosts are highly complex. As more is learned concerning the nature of molecules that confer virulence on C. albicans and those that are involved with defence of the host against Candida, the apparent complexity of the interactions tends to increase rather than decrease. The most common approach to elucidation of virulence attributes and defence mechanisms has been to study the lethality for small animals of intravenously injected yeasts that have been mutated or otherwise perturbed in terms of the function of a putative virulence factor. However, such approaches will need to be refined in the future to ensure that no subtle virulence attributes are overlooked and to define as fully as possible the role of individual host and fungus factors in the infectious process. Candida infections arise as a sequence of steps on a time scale. Adhesion to an epithelial surface initiates the process and colonization of that surface is the second step. The host and fungal factors involved in these stages are unlikely to be exactly the same as those required for penetration of epithelial surfaces. Such penetration is the limit of the infectious process in most instances (with superficial Candida infections as the result) since C. albieans is normally incapable of further invasion of the immunologically intact host. However, in situations where the fungus is able to penetrate to release propagules into the bloodstream, it must necessarily express those attributes that defend it against blood-borne cellular defences and against fungal inhibitors in plasma. To cause disseminated disease, the fungal cells must express the factors necessary for endothelial penetration and tissue invasion. At each step of the process, different panels of host and fungal components can be postulated as playing a predominant role: no host or fungal molecules (or other factors) have so far been demonstrated experimentally to be essential at a particular stage of the infectious pathway. However, clinical observation has established beyond reasonable doubt that intact cellular immune mechanisms are essential for defence of superficial sites, since chronic superficial Candida infections arise predominantly in patients with definable T-lymphocyte deficiencies (e.g. in HIV infection). Conversely, disseminated Candida infections usually require a netropenic host, suggesting that intact phagocytic functions are of major importance in defence of deeper sites. |
Databáze: | OpenAIRE |
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