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Antimicrobial Agents and Chemotherapy, April 1999, p. 763-768, Vol. 43, No. 4
0066-4804/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Effects of Azole Antifungal Drugs on the Transition from Yeast Cells to Hyphae in Susceptible and Resistant Isolates of the Pathogenic Yeast Candida albicans

Kien C. Ha and Theodore C. White*

Department of Pathobiology, School of Public Health and Community Medicine, University of Washington, and the Seattle Biomedical Research Institute, Seattle, Washington

Received 17 September 1998/Returned for modification 23 December 1998/Accepted 13 January 1999

Oral infections caused by the yeast Candida albicans are some of the most frequent and earliest opportunistic infections in human immunodeficiency virus-infected patients. The widespread use of azole antifungal drugs has led to the development of drug resistance, creating a major problem in the treatment of yeast infections in AIDS patients and other immunocompromised individuals. Several molecular mechanisms that contribute to drug resistance have been identified. In C. albicans, the ability to morphologically switch from yeast cells (blastospores) to filamentous forms (hyphae) is an important virulence factor which contributes to the dissemination of Candida in host tissues and which promotes infection and invasion. A positive correlation between the level of antifungal drug resistance and the ability to form hyphae in the presence of azole drugs has been identified. Under hypha-inducing conditions in the presence of an azole drug, resistant clinical isolates form hyphae, while susceptible yeast isolates do not. This correlation is observed in a random sample from a population of susceptible and resistant isolates and is independent of the mechanisms of resistance. 35S-methionine incorporation suggests that growth inhibition is not sufficient to explain the inhibition of hyphal formation, but it may contribute to this inhibition.

* Corresponding author. Mailing address: Seattle Biomedical Research Institute, 4 Nickerson St., Suite 200, Seattle, WA 98109-1651. Phone: (206) 284-8846, ext. 344. Fax: (206) 284-0313. E-mail: tedwhite{at}u.washington.edu.

Antimicrobial Agents and Chemotherapy, April 1999, p. 763-768, Vol. 43, No. 4
0066-4804/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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