Virulence Factors and Azole-Resistant Mechanism of Candida Tropicalis Isolated from Candidemia

Background Limited knowledge exists on the virulence factors of Candida tropicalis and the mechanisms of azole resistance that lead to an intensified pathogenicity and treatment failure. We aimed to evaluate the virulence factors and molecular mechanisms of azole resistance among C. tropicalis isola...

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Veröffentlicht in:Mycopathologia (1975) 2021-12, Vol.186 (6), p.847-856
Hauptverfasser: Sasani, Elahe, Yadegari, Mohammad Hossein, Khodavaisy, Sadegh, Rezaie, Sassan, Salehi, Mohammadreza, Getso, Muhammad Ibrahim
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container_issue 6
container_start_page 847
container_title Mycopathologia (1975)
container_volume 186
creator Sasani, Elahe
Yadegari, Mohammad Hossein
Khodavaisy, Sadegh
Rezaie, Sassan
Salehi, Mohammadreza
Getso, Muhammad Ibrahim
description Background Limited knowledge exists on the virulence factors of Candida tropicalis and the mechanisms of azole resistance that lead to an intensified pathogenicity and treatment failure. We aimed to evaluate the virulence factors and molecular mechanisms of azole resistance among C. tropicalis isolated from patients with candidemia. Materials and Methods Several virulence factors, including extracellular enzymatic activities, cell surface hydrophobicity (CSH), and biofilm formation, were evaluated. Antifungal susceptibility pattern and expression level of ERG11 , UPC2 , MDR1 , and CDR1 genes of eight (4 fluconazole resistance and 4 fluconazole susceptible) clinical C. tropicalis isolates were assessed. The correlation between the virulence factors and antifungal susceptibility patterns was analyzed. Results During a 4 year study, forty-five C. tropicalis isolates were recovered from candidemia patients. The isolates expressed different frequencies of virulence determinants as follows: coagulase 4 (8.9%), phospholipase 5 (11.1%), proteinase 31 (68.9%), esterase 43 (95.6%), hemolysin 44 (97.8%), biofilm formation 45 (100%) and CSH 45(100%). All the isolates were susceptible to amphotericin B and showed the highest resistance to voriconazole. There was a significant positive correlation between micafungin minimum inhibitory concentrations (MICs) and hemolysin production ( r s  = 0.316). However, we found a negative correlation between fluconazole MICs and esterase production ( r s  = −0.383). We observed the high expression of ERG11 and UPC2 genes in fluconazole-resistant C. tropicalis isolates. Conclusion C. tropicalis isolated from candidemia patients extensively displayed capacities for biofilm formation, hemolysis, esterase activity, and hydrophobicity. In addition, the overexpression of ERG11 and UPC2 genes was considered one of the possible mechanisms of azole resistance.
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We aimed to evaluate the virulence factors and molecular mechanisms of azole resistance among C. tropicalis isolated from patients with candidemia. Materials and Methods Several virulence factors, including extracellular enzymatic activities, cell surface hydrophobicity (CSH), and biofilm formation, were evaluated. Antifungal susceptibility pattern and expression level of ERG11 , UPC2 , MDR1 , and CDR1 genes of eight (4 fluconazole resistance and 4 fluconazole susceptible) clinical C. tropicalis isolates were assessed. The correlation between the virulence factors and antifungal susceptibility patterns was analyzed. Results During a 4 year study, forty-five C. tropicalis isolates were recovered from candidemia patients. The isolates expressed different frequencies of virulence determinants as follows: coagulase 4 (8.9%), phospholipase 5 (11.1%), proteinase 31 (68.9%), esterase 43 (95.6%), hemolysin 44 (97.8%), biofilm formation 45 (100%) and CSH 45(100%). All the isolates were susceptible to amphotericin B and showed the highest resistance to voriconazole. There was a significant positive correlation between micafungin minimum inhibitory concentrations (MICs) and hemolysin production ( r s  = 0.316). However, we found a negative correlation between fluconazole MICs and esterase production ( r s  = −0.383). We observed the high expression of ERG11 and UPC2 genes in fluconazole-resistant C. tropicalis isolates. Conclusion C. tropicalis isolated from candidemia patients extensively displayed capacities for biofilm formation, hemolysis, esterase activity, and hydrophobicity. In addition, the overexpression of ERG11 and UPC2 genes was considered one of the possible mechanisms of azole resistance.</description><identifier>ISSN: 0301-486X</identifier><identifier>EISSN: 1573-0832</identifier><identifier>DOI: 10.1007/s11046-021-00580-y</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Amphotericin B ; Antifungal agents ; Biofilms ; Biomedical and Life Sciences ; Candidemia ; Cell surface ; Coagulase ; Complementarity-determining region 1 ; Enzymatic activity ; Enzymes ; Esterase ; Eukaryotic Microbiology ; Fluconazole ; Hydrophobicity ; Life Sciences ; MDR1 protein ; Medical Microbiology ; Micafungin ; Microbial Ecology ; Microbiology ; Molecular modelling ; Original Article ; Pathogenicity ; Patients ; Phospholipases ; Plant Sciences ; Proteinase ; Virulence factors ; Voriconazole</subject><ispartof>Mycopathologia (1975), 2021-12, Vol.186 (6), p.847-856</ispartof><rights>The Author(s), under exclusive licence to Springer Nature B.V. 2021</rights><rights>COPYRIGHT 2021 Springer</rights><rights>The Author(s), under exclusive licence to Springer Nature B.V. 2021.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c497t-9f6ab9ac03daba072ec432d293d8d1d83b091334b9a75c06296d71c0b65e9f783</citedby><cites>FETCH-LOGICAL-c497t-9f6ab9ac03daba072ec432d293d8d1d83b091334b9a75c06296d71c0b65e9f783</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11046-021-00580-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11046-021-00580-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51298</link.rule.ids></links><search><creatorcontrib>Sasani, Elahe</creatorcontrib><creatorcontrib>Yadegari, Mohammad Hossein</creatorcontrib><creatorcontrib>Khodavaisy, Sadegh</creatorcontrib><creatorcontrib>Rezaie, Sassan</creatorcontrib><creatorcontrib>Salehi, Mohammadreza</creatorcontrib><creatorcontrib>Getso, Muhammad Ibrahim</creatorcontrib><title>Virulence Factors and Azole-Resistant Mechanism of Candida Tropicalis Isolated from Candidemia</title><title>Mycopathologia (1975)</title><addtitle>Mycopathologia</addtitle><description>Background Limited knowledge exists on the virulence factors of Candida tropicalis and the mechanisms of azole resistance that lead to an intensified pathogenicity and treatment failure. We aimed to evaluate the virulence factors and molecular mechanisms of azole resistance among C. tropicalis isolated from patients with candidemia. Materials and Methods Several virulence factors, including extracellular enzymatic activities, cell surface hydrophobicity (CSH), and biofilm formation, were evaluated. Antifungal susceptibility pattern and expression level of ERG11 , UPC2 , MDR1 , and CDR1 genes of eight (4 fluconazole resistance and 4 fluconazole susceptible) clinical C. tropicalis isolates were assessed. The correlation between the virulence factors and antifungal susceptibility patterns was analyzed. Results During a 4 year study, forty-five C. tropicalis isolates were recovered from candidemia patients. The isolates expressed different frequencies of virulence determinants as follows: coagulase 4 (8.9%), phospholipase 5 (11.1%), proteinase 31 (68.9%), esterase 43 (95.6%), hemolysin 44 (97.8%), biofilm formation 45 (100%) and CSH 45(100%). All the isolates were susceptible to amphotericin B and showed the highest resistance to voriconazole. There was a significant positive correlation between micafungin minimum inhibitory concentrations (MICs) and hemolysin production ( r s  = 0.316). However, we found a negative correlation between fluconazole MICs and esterase production ( r s  = −0.383). We observed the high expression of ERG11 and UPC2 genes in fluconazole-resistant C. tropicalis isolates. Conclusion C. tropicalis isolated from candidemia patients extensively displayed capacities for biofilm formation, hemolysis, esterase activity, and hydrophobicity. 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We aimed to evaluate the virulence factors and molecular mechanisms of azole resistance among C. tropicalis isolated from patients with candidemia. Materials and Methods Several virulence factors, including extracellular enzymatic activities, cell surface hydrophobicity (CSH), and biofilm formation, were evaluated. Antifungal susceptibility pattern and expression level of ERG11 , UPC2 , MDR1 , and CDR1 genes of eight (4 fluconazole resistance and 4 fluconazole susceptible) clinical C. tropicalis isolates were assessed. The correlation between the virulence factors and antifungal susceptibility patterns was analyzed. Results During a 4 year study, forty-five C. tropicalis isolates were recovered from candidemia patients. The isolates expressed different frequencies of virulence determinants as follows: coagulase 4 (8.9%), phospholipase 5 (11.1%), proteinase 31 (68.9%), esterase 43 (95.6%), hemolysin 44 (97.8%), biofilm formation 45 (100%) and CSH 45(100%). All the isolates were susceptible to amphotericin B and showed the highest resistance to voriconazole. There was a significant positive correlation between micafungin minimum inhibitory concentrations (MICs) and hemolysin production ( r s  = 0.316). However, we found a negative correlation between fluconazole MICs and esterase production ( r s  = −0.383). We observed the high expression of ERG11 and UPC2 genes in fluconazole-resistant C. tropicalis isolates. Conclusion C. tropicalis isolated from candidemia patients extensively displayed capacities for biofilm formation, hemolysis, esterase activity, and hydrophobicity. In addition, the overexpression of ERG11 and UPC2 genes was considered one of the possible mechanisms of azole resistance.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><doi>10.1007/s11046-021-00580-y</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record>
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subjects Amphotericin B
Antifungal agents
Biofilms
Biomedical and Life Sciences
Candidemia
Cell surface
Coagulase
Complementarity-determining region 1
Enzymatic activity
Enzymes
Esterase
Eukaryotic Microbiology
Fluconazole
Hydrophobicity
Life Sciences
MDR1 protein
Medical Microbiology
Micafungin
Microbial Ecology
Microbiology
Molecular modelling
Original Article
Pathogenicity
Patients
Phospholipases
Plant Sciences
Proteinase
Virulence factors
Voriconazole
title Virulence Factors and Azole-Resistant Mechanism of Candida Tropicalis Isolated from Candidemia
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