-
Je něco špatně v tomto záznamu ?
Prevalence of Antifungal Resistance, Genetic Basis of Acquired Azole and Echinocandin Resistance, and Genotyping of Candida krusei Recovered from an International Collection
HO. Khalifa, V. Hubka, A. Watanabe, M. Nagi, Y. Miyazaki, T. Yaguchi, K. Kamei
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, práce podpořená grantem
Freely Accessible Science Journals od 1995 do Před 6 měsíci
PubMed Central od 1972 do Před 6 měsíci
Europe PubMed Central od 1972 do Před 6 měsíci
Open Access Digital Library od 1972-01-01
Open Access Digital Library od 1972-01-01
Odkazy
PubMed
34871096
DOI
10.1128/aac.01856-21
Knihovny.cz E-zdroje
- MeSH
- antifungální látky farmakologie terapeutické užití MeSH
- azoly * farmakologie MeSH
- echinokandiny * farmakologie MeSH
- fungální léková rezistence genetika MeSH
- genotyp MeSH
- mikrobiální testy citlivosti MeSH
- Pichia MeSH
- prevalence MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
This study was designed to evaluate the prevalence of antifungal resistance, genetic mechanisms associated with in vitro induction of azole and echinocandin resistance and genotyping of Candida krusei, which is intrinsically resistant to fluconazole and is recovered from clinical and nonclinical sources from different countries. Our results indicated that all the isolates were susceptible or had the wild phenotype (WT) to azoles, amphotericin B, and only 1.27% showed non-WT for flucytosine. Although 70.88% of the isolates were resistant to caspofungin, none of them were categorized as echinocandin-resistant as all were susceptible to micafungin and no FKS1 hot spot 1 (HS1) or HS2 mutations were detected. In vitro induction of azole and echinocandin resistance confirmed the rapid development of resistance at low concentrations of fluconazole (4 μg/ml), voriconazole (0.06 μg/ml), and micafungin (0.03 μg/ml), with no difference between clinical and nonclinical isolates in the resistance development. Overexpression of ABC1 gene and FKS1 HS1 mutations were the major mechanisms responsible for azole and echinocandin resistance, respectively. Genotyping of our 79 isolates coupled with 217 other isolates from different sources and geography confirmed that the isolates belong to two main subpopulations, with isolates from human clinical material and Asia being more predominant in cluster 1, and environmental and animals isolates and those from Europe in cluster 2. Our results are of critical concern, since realizing that the C. krusei resistance mechanisms and their genotyping are crucial for guiding specific therapy and for exploring the potential infection source.
Antimicrobial Resistance Research Center National Institute of Infectious Diseases Tokyo Japan
Department of Botany Faculty of Science Charles University Prague Czech Republic
Department of Fungal Infection National Institute of Infectious Diseases Tokyo Japan
Division of Bio resources Medical Mycology Research Center Chiba University Chiba Japan
Division of Clinical Research Medical Mycology Research Center Chiba University Chiba Japan
- 000
- 00000naa a2200000 a 4500
- 001
- bmc22010990
- 003
- CZ-PrNML
- 005
- 20220506130457.0
- 007
- ta
- 008
- 220425s2022 xxu f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.1128/AAC.01856-21 $2 doi
- 035 __
- $a (PubMed)34871096
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a xxu
- 100 1_
- $a Khalifa, Hazim O $u Division of Clinical Research, Medical Mycology Research Center, Chiba University, Chiba, Japan $u Department of Pharmacology, Faculty of Veterinary Medicine, Kafrelsheikh University, Kafr El-Sheikh, Egypt $1 https://orcid.org/0000000198619693
- 245 10
- $a Prevalence of Antifungal Resistance, Genetic Basis of Acquired Azole and Echinocandin Resistance, and Genotyping of Candida krusei Recovered from an International Collection / $c HO. Khalifa, V. Hubka, A. Watanabe, M. Nagi, Y. Miyazaki, T. Yaguchi, K. Kamei
- 520 9_
- $a This study was designed to evaluate the prevalence of antifungal resistance, genetic mechanisms associated with in vitro induction of azole and echinocandin resistance and genotyping of Candida krusei, which is intrinsically resistant to fluconazole and is recovered from clinical and nonclinical sources from different countries. Our results indicated that all the isolates were susceptible or had the wild phenotype (WT) to azoles, amphotericin B, and only 1.27% showed non-WT for flucytosine. Although 70.88% of the isolates were resistant to caspofungin, none of them were categorized as echinocandin-resistant as all were susceptible to micafungin and no FKS1 hot spot 1 (HS1) or HS2 mutations were detected. In vitro induction of azole and echinocandin resistance confirmed the rapid development of resistance at low concentrations of fluconazole (4 μg/ml), voriconazole (0.06 μg/ml), and micafungin (0.03 μg/ml), with no difference between clinical and nonclinical isolates in the resistance development. Overexpression of ABC1 gene and FKS1 HS1 mutations were the major mechanisms responsible for azole and echinocandin resistance, respectively. Genotyping of our 79 isolates coupled with 217 other isolates from different sources and geography confirmed that the isolates belong to two main subpopulations, with isolates from human clinical material and Asia being more predominant in cluster 1, and environmental and animals isolates and those from Europe in cluster 2. Our results are of critical concern, since realizing that the C. krusei resistance mechanisms and their genotyping are crucial for guiding specific therapy and for exploring the potential infection source.
- 650 _2
- $a zvířata $7 D000818
- 650 _2
- $a antifungální látky $x farmakologie $x terapeutické užití $7 D000935
- 650 12
- $a azoly $x farmakologie $7 D001393
- 650 _2
- $a fungální léková rezistence $x genetika $7 D025141
- 650 12
- $a echinokandiny $x farmakologie $7 D054714
- 650 _2
- $a genotyp $7 D005838
- 650 _2
- $a mikrobiální testy citlivosti $7 D008826
- 650 _2
- $a Pichia $7 D010843
- 650 _2
- $a prevalence $7 D015995
- 655 _2
- $a časopisecké články $7 D016428
- 655 _2
- $a práce podpořená grantem $7 D013485
- 700 1_
- $a Hubka, Vit $u Department of Botany, Faculty of Science, Charles University, Prague, Czech Republic $u Laboratory of Fungal Genetics and Metabolism, Institute of Microbiology, Czech Academy of Sciences, Prague, Czech Republic $u Division of Bio-resources, Medical Mycology Research Center, Chiba University, Chiba, Japan $1 https://orcid.org/0000000345836496 $7 mzk2016904736
- 700 1_
- $a Watanabe, Akira $u Division of Clinical Research, Medical Mycology Research Center, Chiba University, Chiba, Japan $1 https://orcid.org/0000000230572937
- 700 1_
- $a Nagi, Minoru $u Department of Fungal Infection, National Institute of Infectious Diseases, Tokyo, Japan $u Antimicrobial Resistance Research Center, National Institute of Infectious Diseases, Tokyo, Japan
- 700 1_
- $a Miyazaki, Yoshitsugu $u Department of Fungal Infection, National Institute of Infectious Diseases, Tokyo, Japan $1 https://orcid.org/0000000189420869
- 700 1_
- $a Yaguchi, Takashi $u Division of Bio-resources, Medical Mycology Research Center, Chiba University, Chiba, Japan
- 700 1_
- $a Kamei, Katsuhiko $u Division of Clinical Research, Medical Mycology Research Center, Chiba University, Chiba, Japan
- 773 0_
- $w MED00009215 $t Antimicrobial agents and chemotherapy $x 1098-6596 $g Roč. 66, č. 2 (2022), s. e0185621
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/34871096 $y Pubmed
- 910 __
- $a ABA008 $b sig $c sign $y p $z 0
- 990 __
- $a 20220425 $b ABA008
- 991 __
- $a 20220506130450 $b ABA008
- 999 __
- $a ok $b bmc $g 1788882 $s 1162188
- BAS __
- $a 3
- BAS __
- $a PreBMC
- BMC __
- $a 2022 $b 66 $c 2 $d e0185621 $e 20211206 $i 1098-6596 $m Antimicrobial agents and chemotherapy $n Antimicrob Agents Chemother $x MED00009215
- LZP __
- $a Pubmed-20220425