Clonal and Spontaneous Origins of Fluconazole Resistance in Candida albicans
Open accessAbstract
The genotypes and susceptibilities to fluconazole of 78 strains of the human pathogenic yeast Candida albicans were compared. The strains comprised two sets of samples from Durham, N.C.: one from patients infected with the human immunodeficiency virus (HIV) and the other from healthy volunteers. For each strain, the MIC of fluconazole was determined by the standard National Committee for Clinical Laboratory Standards protocol. Genotypes were determined by PCR fingerprinting with five separate primers. The analysis revealed little evidence for genotypic clustering according to HIV status or body site. However, a small group of fluconazole-resistant strains isolated from patients infected with HIV formed a distinct cluster. In addition, two fluconazole-resistant strains were isolated from individuals who never took fluconazole, one from a patient infected with HIV and the other from a healthy person. The results suggest both clonal and spontaneous origins of fluconazole resistance in C. albicans.
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Azole resistance for C. albicans is reported sporadically in healthy adults.
“However, azole resistance for this species is now well described among HIV-infected individuals with recurrent oropharyngeal candidiasis and is also reported sporadically in critically ill adults with invasive candidiasis [25] or in healthy adults [26].”
From Guidelines for Treatment of Candidiasis (2004) · cites this paper as [26]
Azole resistance for C. albicans is well described among HIV-infected individuals with recurrent oropharyngeal candidiasis.
“However, azole resistance for this species is now well described among HIV-infected individuals with recurrent oropharyngeal candidiasis and is also reported sporadically in critically ill adults with invasive candidiasis [25] or in healthy adults [26].”
From Guidelines for Treatment of Candidiasis (2004) · cites this paper as [26]
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Self-citation
- Authors
- Xu, J., Ramos, A. R., Vilgalys, R., & Mitchell, T. G.
- Affiliations
- Duke University (US)
- Venue
- Journal of Clinical Microbiology
- Publisher
- American Society for Microbiology
- Published
- 2000-03
- Volume
- 38
- Issue
- 3
- Pages
- 1214-1220
- ISSN
- 0095-1137 (ISSN-L)
- 1098-660X
- PMC
- PMC86380
- OpenAlex
- W2122879168
- Cited by
- 123
- References
- 26
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 1 · 2022: 3 · 2021: 3 · 2020: 1 · 2019: 3 · 2018: 5 · 2017: 4 · 2016: 6 · 2015: 4 · 2014: 5 · 2013: 6 · 2012: 1
- FWCI
- 7.55
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Clinical Microbiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ai028836-08)
- National Institute of Allergy and Infectious Diseases (AI 28836)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Yeasts and Rust Fungi Studies
- Keywords
- Candida albicans, fluconazole resistance, antifungal resistance, clonal origin, spontaneous resistance, HIV infection, PCR fingerprinting, minimum inhibitory concentration
- MeSH terms
- Antifungal Agents, Candida albicans, Candidiasis, Candidiasis, Oral, Candidiasis, Vulvovaginal, DNA, Fungal, Drug Resistance, Microbial, Female, Genotype, Humans, Phylogeny, HIV Infections, Fluconazole, Polymerase Chain Reaction, AIDS-Related Opportunistic Infections
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