Mechanisms of Antifungal Drug Resistance in Candida Dubliniensis

Abstract

Candida dubliniensis was first described in 1995 and is the most closely related species to the predominant human fungal pathogen Candida albicans. C. dubliniensis is significantly less prevalent and less pathogenic than C. albicans and is primarily associated with infections in HIV-infected individuals and other immunocompromised cohorts. The population structure of C. dubliniensis consists of three well-defined major clades and is significantly less diverse than C. albicans. The majority of C. dubliniensis isolates are susceptible to antifungal drugs commonly used to treat Candida infections. To date only two major patterns of antifungal drug resistance have been identified and the molecular mechanisms of these are very similar to the resistance mechanisms that have been described previously in C. albicans. However, significant differences are evident in the predominant antifungal drug mechanisms employed by C. dubliniensis, differences that reflect its more clonal nature, its lower prevalence and characteristics of its genome, the complete sequence of which has only recently been determined.

Keywords:

• 5-fluorocytosine resistance
• antifungal drug resistance
• Candida dubliniensis
• CdCDR1
• CdERG11
• CdERG3
• CdFCA1
• CdMDR1
• CdMRR1
• fluconazole resistance
• resistance mechanisms

Financial & competing interests disclosure

Work in the authors‘ laboratory was supported by Irish Health Research Board grant Nos. RP41/96, RP04/97, RP04/99, RP05/97, RP/05/2, Science Foundation Ireland PI grant No. 04/IN3/B463 and by the Dublin Dental School & Hospital Microbiology Research Unit. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

Work in the authors‘ laboratory was supported by Irish Health Research Board grant Nos. RP41/96, RP04/97, RP04/99, RP05/97, RP/05/2, Science Foundation Ireland PI grant No. 04/IN3/B463 and by the Dublin Dental School & Hospital Microbiology Research Unit. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.