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Virulence Factors Contributing to Pathogenicity of Candida tropicalis and Its Antifungal Susceptibility Profile
The incidence of invasive candidiasis has increased over the past few decades. Although Candida albicans remains by far the most common species encountered, in recent years shift towards non-albicans Candida species like Candida tropicalis is noted. Here in this study we determined the virulence fac...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3996979/ https://www.ncbi.nlm.nih.gov/pubmed/24803934 http://dx.doi.org/10.1155/2014/456878 |
Sumario: | The incidence of invasive candidiasis has increased over the past few decades. Although Candida albicans remains by far the most common species encountered, in recent years shift towards non-albicans Candida species like Candida tropicalis is noted. Here in this study we determined the virulence factors and antifungal susceptibility profile of 125 C. tropicalis isolated from various clinical specimens. Biofilm formation was seen in 53 (42.4%) isolates. Coagulase production was noted in 18 (14.4%) isolates. Phospholipase enzyme was the major virulent factor produced by C. tropicalis isolates. A total of 39 biofilm forming isolates showed phospholipase activity. Proteinase activity was demonstrated by 65 (52%) isolates. A total of 38 (30.4%) isolates showed haemolytic activity. Maximum isolates demonstrated resistance to fluconazole. Fluconazole resistance was more common in C. tropicalis isolated from blood cultures. Antifungal resistance was more in isolates possessing the ability to produce phospholipase and biofilm. C. tropicalis exhibit a great degree of variation not only in their pathogenicity but also in their antifungal susceptibility profile. The identification of virulence attributes specific for each species and their correlation with each other will aid in the understanding of the pathogenesis of infection. |
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