Malassezia spp. and Candida spp. from patients with psoriasis exhibit reduced susceptibility to antifungals.

INTRODUCTION: Psoriasis is a chronic inflammatory disease that affects over 125 million people worldwide. Many studies have shown the importance of the microbiome for psoriasis exacerbation. AIM: Explore the fungal load and species composition of cultivable yeasts on the skin of psoriatic patients (PP) and healthy volunteers living in a tropical area and evaluate the susceptibility to antifungals. METHODOLOGY: A cross-sectional study with 61 participants (35 patients and 26 healthy controls) was performed during August 2018 and May 2019. Clinical data were collected from patient interviewing and/or medical records review. Samples were collected by swabbing in up to five anatomic sites. Suggestive yeast colonies were counted and further identified by phenotypical tests, PCR-REA, and/or MALDI-TOF. Susceptibility of Malassezia spp. and Candida spp. to azoles, terbinafine, and amphotericin B was evaluated by broth microdilution. RESULTS: Nearly 50% of the patients had moderate to severe psoriasis, and plaque-type psoriasis was the most common clinical form. Yeast colonies count was significantly more abundant among PP than healthy controls. Malassezia and Candida were the most abundant genus detected in all participants. Higher MIC values for ketoconazole and terbinafine were observed in Malassezia strains obtained from PP. Approximately 42% of Candida isolates from PP showed resistance to itraconazole in contrast to 12.5% of isolates from healthy controls. MIC values for fluconazole and amphotericin B were significantly different among Candida isolates from PP and healthy individuals. CONCLUSION: This study showed that Malassezia and Candida strains from PP presented higher MIC values to widespread antifungal drugs than healthy individuals.

Heterologous extracellular DNA facilitates the development of Trichosporon asahii and T. inkin biofilms and enhances their tolerance to antifungals.

Trichosporon asahii and T. inkin are emergent agents of deep-seated and disseminated infections in immunocompromised patients. The present study aimed to investigate the role of extracellular DNA (eDNA) and the enzyme deoxyribonuclease (DNase) on the structure of T. asahii and T. inkin biofilms, as well as to examine their effect on the susceptibility to antifungals. Biofilms reached maturity at 48 h; eDNA concentration in the supernatant increased over time (6 < 24 h < 48h). Exogenous eDNA increased biomass of Trichosporon biofilms at all stages of development, enhanced their tolerance to antifungals and improved their structural complexity. DNase reduced biomass, biovolume and thickness of Trichosporon biofilms, thereby rendering them more susceptibility to voriconazole. The results suggest the relevance of eDNA in the structure and antifungal susceptibility of Trichosporon biofilms and highlight the potential of DNase as adjuvant in biofilm control.

Proposal for a microcosm biofilm model for the study of vulvovaginal candidiasis.

This study proposes a microcosm biofilm (MiB) model for the study of vulvovaginal candidiasis (VVC). Different conditions that mimic the vaginal environment were tested for MiB formation. The best growth conditions were obtained with samples incubated in vaginal fluid simulator medium pH 4.5 at 35 °C under a microaerophilic atmosphere. MiBs were evaluated for growth kinetics, fluconazole susceptibility and morphology. Samples containing high numbers of bacteria were analyzed for metagenomics. At 48 h, MiBs presented a higher cell density (CFU ml-1), a higher biomass and tolerance to fluconazole than their corresponding monospecies biofilms. Morphological analysis of MiBs revealed blastoconidia preferentially adhered to epithelial cells. Abundant Lactobacillus spp. were detected in two clinical samples; their MiBs showed a lower biomass and a higher fluconazole susceptibility. The proposed model proved to be a useful tool for the study of the complex microbial relationship in the vaginal environment, and may help to find new strategies for VVC control.