Pathogenesis and treatment of oral candidosis

Abstract

Oral infections caused by yeast of the genus Candida and particularly Candida albicans (oral candidoses) have been recognised throughout recorded history. However, since the 1980s a clear surge of interest and associated research into these infections have occurred. This has largely been due to an increased incidence of oral candidosis over this period, primarily because of the escalation in HIV-infection and the AIDS epidemic. In addition, changes in medical practice leading to a greater use of invasive clinical procedures and a more widespread use of immunosuppressive therapies have also contributed to the problem. Whilst oral candidosis has previously been considered to be a disease mainly of the elderly and very young, its occurrence throughout the general population is now recognised. Candida are true 'opportunistic pathogens' and only instigate oral infection when there is an underlying predisposing condition in the host. Treatment of these infections has continued (and in some regards continues) to be problematic because of the potential toxicity of traditional antifungal agents against host cells. The problem has been compounded by the emergence of Candida species other than C. albicans that have inherent resistance against traditional antifungals. The aim of this review is to give the reader a contemporary overview of oral candidosis, the organisms involved, and the management strategies that are currently employed or could be utilised in the future.

Keywords: Candida; oral candidosis.

Fig. 1

Clinical presentation of the primary forms of oral candidosis. (a) acute pseudomembranous candidosis; (b) chronic erythematous candidosis; (c) acute erythematous candidosis; and (d) chronic hyperplastic candidosis.

Fig. 2

Periodic Acid Schiff stained biopsy section of chronic hyperplastic candidosis. Typical invading hypha indicated by arrow.

Fig. 3

Calcofluor white stained Candida albicans showing true hyphae (*) and pseudohyphae (+).