Abstract
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. 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. During a 4year 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 (rs = 0.316). However, we found a negative correlation between fluconazole MICs and esterase production (rs = -0.383). We observed the high expression of ERG11 and UPC2 genes in fluconazole-resistant C. tropicalis isolates. 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.
Highlights
Nosocomial bloodstream infections (BSIs) caused by Candida spp are the fourth and sixth causes of BSIs in the USA and Europe, respectively [1,2,3,4]
C. tropicalis isolated from candidemia patients extensively displayed capacities for biofilm formation, hemolysis, esterase activity, and hydrophobicity
Some factors that contributed to azole resistance of Candida species contain mutations and/or overexpression of ERG11, UPC2, CDR1(encoding for efflux protein of ATP binding-cassette (ABC) family), and MDR1(encoding for efflux protein of major facilitator superfamily (MFS) family) [16, 17]
Summary
Nosocomial bloodstream infections (BSIs) caused by Candida spp are the fourth and sixth causes of BSIs in the USA and Europe, respectively [1,2,3,4]. Many virulence factors have been represented for candidemia establishment including extracellular secreted enzymes (phospholipase, esterase, coagulase, and proteinase), hemolytic factor, and biofilm formation [11, 12]. These factors can intensify candidemia by Candida escape from the immune system to damage the host tissue [13]. This study aimed to evaluate the virulence factors (extracellular enzymatic activities, cell surface hydrophobicity, and biofilm formation), the pattern of antifungal susceptibility and expression of ERG11, UPC2, MDR1, and CDR1 genes in C. tropicalis isolated from candidemia patients in Tehran, Iran. We aimed to evaluate the virulence factors and the molecular mechanisms of azole resistance among C. tropicalis isolated from bloodstream infection
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