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J Reprod Med. 1989 Aug;34(8 Suppl):572-9; discussion 579-80.

Pathophysiology of vulvovaginal candidiasis.

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1
Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201.

Abstract

Women with infrequent episodes of candidal vaginitis frequently have an identifiable cause, but those with chronic and recurrent candidal vaginitis rarely have recognizable precipitating or causal factors. Although an analysis of vaginal yeast isolated from women with recurrent candidal vaginitis reveals a higher percentage of non-albicans species of Candida, resistance to imidazoles is rarely responsible for the recurrent or chronic cases. Strain typing of sequential clinical isolates suggests a pattern of vaginal relapse rather than of frequent vaginal reinfection. Attempts to reduce attacks by treating sexual partners and suppressing a putative gastrointestinal tract focus have failed in the past. The results of immunologic studies suggest the possibility of an acquired Candida antigen-specific immunologic deficiency that results in uncontrolled vaginal Candida proliferation and, hence, repeated clinical attacks. The recent report of normal T-lymphocyte suppression of Candida germ tube production and, hence, inhibition of Candida virulence supports the immunologic hypothesis. Moreover, observations of high-frequency, genetically controlled switching colonies of Candida albicans, accompanied by enhanced virulence and invasive potential of the yeast, may provide an explanation for the recurrent nature of candidal vaginitis in certain women.

PMID:
2677361
[Indexed for MEDLINE]

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