Abstract
The factors enabling Candida spp. infections are secretion of hydrolytic enzymes, adherence to surfaces, biofilm formation or morphological transition, and fitness attributes. The aim of this study was to investigate the correlation between known extracellular virulence factors and survival of Galleria mellonella larvae infected with clinical Candida. The 25 isolates were tested and the activity of proteinases among 24/24, phospholipases among 7/22, esterases among 14/23, hemolysins among 18/24, and biofilm formation ability among 18/25 isolates was confirmed. Pathogenicity investigation using G. mellonella larvae as host model demonstrated that C. albicans isolates and C. glabrata isolate were the most virulent and C. krusei isolates were avirulent. C. parapsilosis virulence was identified as varied, C. inconspicua were moderately virulent, and one C. palmioleophila isolate was of low virulence and the remaining isolates of this species were moderately virulent. According to our study, virulence of Candida isolates is related to the expression of proteases, hemolysins, and esterases.
Highlights
Candida spp. are the part of natural microbiota of healthy individuals
The presented research are based on the group of 25 Candida isolates (15 C. albicans, 1 C. glabrata, 1 C. inconspicua, 1 C. krusei, 3 C. palmioleophila, and 4 C. parapsilosis)
The virulence factors were identified in different Candida spp. such as: C. albicans [39], C. auris [40], C. parapsilosis complex [41], C. tropicalis [4], C. krusei, and C. glabrata [42]
Summary
Candida spp. are the part of natural microbiota of healthy individuals. Under conditions of host weakness, Candida isolates can become opportunist. Confirmed that endogenous isolates are the major cause of Candida infections [1]. Those infections are the fourth most common hospital-acquired systemic infections in the United States with mortality rates of up to. Progress of medicine paradoxically is a reason of increasing number of opportunistic Candida infections. Candida spp. facilitated its invasion and infections by expression of virulence factors (secretion of hydrolytic enzymes, adherence to surfaces, biofilm formation or morphological transition—Figure 1) and fitness attributes [4]
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