Fluconazole resistance in Candida species: a current perspective

被引:358
作者
Berkow, Elizabeth L. [1 ]
Lockhart, Shawn R. [1 ]
机构
[1] Ctr Dis Control & Prevent, Mycot Dis Branch, Atlanta, GA USA
关键词
Candida; fluconazole resistance; ERG11; drug efflux; ergosterol; ANTIFUNGAL-DRUG-RESISTANCE; AMINO-ACID SUBSTITUTIONS; AZOLE RESISTANCE; MOLECULAR-MECHANISMS; MULTIDRUG-RESISTANCE; UP-REGULATION; ERG11; GENE; IN-VIVO; ABC TRANSPORTERS; CROSS-RESISTANCE;
D O I
10.2147/IDR.S118892
中图分类号
R51 [传染病];
学科分类号
100401 ;
摘要
Candida albicans and the emerging non-albicans Candida spp. have significant clinical relevance among many patient populations. Current treatment guidelines include fluconazole as a primary therapeutic option for the treatment of these infections, but it is only fungistatic against Candida spp. and both inherent and acquired resistance to fluconazole have been reported. Such mechanisms of resistance include increased drug efflux, alteration or increase in the drug target, and development of compensatory pathways for producing the target sterol, ergosterol. While many mechanisms of resistance observed in C. albicans are also found in the non-albicans species, there are also important and unexpected differences between species. Furthermore, mechanisms of fluconazole resistance in emerging Candida spp., including the global health threat Candida auris, are largely unknown. In order to preserve the utility of one of our fundamental antifungal drugs, fluconazole, it is essential that we fully appreciate the manner by which Candida spp. manifest resistance to it.
引用
收藏
页码:237 / 245
页数:9
相关论文
共 108 条
[91]   Aneuploidy and isochromosome formation in drug-resistant Candida albicans [J].
Selmecki, Anna ;
Forche, Anja ;
Berman, Judith .
SCIENCE, 2006, 313 (5785) :367-370
[92]   Persistent Candida albicans colonization and molecular mechanisms of azole resistance in autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) patients [J].
Siikala, Emilia ;
Rautemaa, Riina ;
Richardson, Malcolm ;
Saxen, Harri ;
Bowyer, Paul ;
Sanglard, Dominique .
JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY, 2010, 65 (12) :2505-2513
[93]   Candida parapsilosis Resistance to Fluconazole: Molecular Mechanisms and In Vivo Impact in Infected Galleria mellonella Larvae [J].
Souza, Ana Carolina R. ;
Fuchs, Beth Burgwyn ;
Pinhati, Henrique M. S. ;
Siqueira, Ricardo A. ;
Hagen, Ferry ;
Meis, Jacques F. ;
Mylonakis, Eleftherios ;
Colombo, Arnaldo L. .
ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, 2015, 59 (10) :6581-6587
[94]   Isolation of a putative Candida albicans transcriptional regulator involved in pleiotropic drug resistance by functional complementation of a pdr1 pdr3 mutation in Saccharomyces cerevisiae [J].
Talibi, D ;
Raymond, M .
JOURNAL OF BACTERIOLOGY, 1999, 181 (01) :231-240
[95]   The A395T Mutation in ERG11 Gene Confers Fluconazole Resistance in Candida tropicalis Causing Candidemia [J].
Tan, Jingwen ;
Zhang, Jinqing ;
Chen, Wei ;
Sun, Yi ;
Wan, Zhe ;
Li, Ruoyu ;
Liu, Wei .
MYCOPATHOLOGIA, 2015, 179 (3-4) :213-218
[96]  
Tavakoli M, 2010, DARU, V18, P276
[97]   The ATP-binding cassette transporter-encoding gene CgSNQ2 is contributing to the CgPDR1-dependent azole resistance of Candida glabrata [J].
Torelli, Riccardo ;
Posteraro, Brunella ;
Ferrari, Selene ;
La Sorda, Marilena ;
Fadda, Giovanni ;
Sanglard, Dominique ;
Sanguinetti, Maurizio .
MOLECULAR MICROBIOLOGY, 2008, 68 (01) :186-201
[98]   Relative Contributions of the Candida albicans ABC Transporters Cdr1p and Cdr2p to Clinical Azole Resistance [J].
Tsao, Sarah ;
Rahkhoodaee, Fariba ;
Raymond, Martine .
ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, 2009, 53 (04) :1344-1352
[99]   CHARACTERIZATION OF AN AZOLE-RESISTANT CANDIDA-GLABRATA ISOLATE [J].
VANDENBOSSCHE, H ;
MARICHAL, P ;
ODDS, FC ;
LEJEUNE, L ;
COENE, MC .
ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, 1992, 36 (12) :2602-2610
[100]   Mechanisms of azole resistance in a clinical isolate of Candida tropicalis [J].
Vandeputte, P ;
Larcher, G ;
Bergès, T ;
Renier, G ;
Chabasse, D ;
Bouchara, JP .
ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, 2005, 49 (11) :4608-4615