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Part of the book series: Molecular and Cell Biology of Human Diseases Series ((Mol. Cell Biol. Hu. Dis.))

Abstract

Candida aibicans and related species represent an ever increasing problem not only in immunocompromised patients (Wey et al., 1988) but also in patients with other predisposing conditions, as well as in apparently healthy individuals (Odds, 1988; Bodey and Feinstein, 1985). These opportunistic pathogens are capable of infecting virtually every tissue of the human body and have been responsible for an increasing number of nosocomial infections (Weber and Rutala, 1988; Isenberg et al., 1989; Burnie et al., 1985; Wey et al., 1988). In HIV-positive individuals, oraloesophageal candidosis represents one of the first signs of symptomatic AIDS (Greenspan, 1988; Syrjanen et al., 1988), and there is preliminary evidence suggesting strain selection and evolution in these patients (Odds et al., 1990). The success of Candida as a pathogen must stem partly from its commensal existence in the natural flora of most individuals and partly from a combination of pathogenic traits. However, for reasons not immediately obvious, but which must include the absence of a reasonable genetic system for experimental investigation (Whelan, 1987), we know little about the epidemiology, etiology and molecular pathology of Candida.

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Soll, D.R. (1992). Molecular biology of Candida pathogenesis. In: Wright, D., Archard, L. (eds) Molecular and Cell Biology of Sexually Transmitted Diseases. Molecular and Cell Biology of Human Diseases Series. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-2384-6_5

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