Molecular epidemiology, in vitro susceptibility and exoenzyme screening of Malassezia clinical isolates

Abstract

Introduction. Malassezia folliculitis (MF) and pityriasis versicolor (PV) are common dermatoses caused by Malassezia species. Their molecular epidemiology, drug susceptibility and exoenzymes are rarely reported in China. Aim. To investigate the molecular epidemiology, drug susceptibility and enzymatic profile of Malassezia clinical isolates. Methodology. Malassezia strains were recovered from MF and PV patients and healthy subjects (HS) and identified by sequencing analysis. The minimum inhibitory concentrations (MICs) of nine antifungals (posaconazole, voriconazole, itraconazole, fluconazole, ketoconazole, miconazole, bifonazole, terbinafine and caspofungin) and tacrolimus, the interactions between three antifungals (itraconazole, ketoconazole and terbinafine) and tacrolimus, and the extracellular enzyme profile were evaluated using broth and checkerboard microdilution and the Api-Zym system, respectively. Results. Among 392 Malassezia isolates from 729 subjects (289 MF, 218 PV and 222 HS), Malassezia furfur and Malassezia globosa accounted for 67.86 and 18.88 %, respectively. M. furfur was the major species in MF and PV patients and HS. Among 60M. furfur and 50M. globosa strains, the MICs for itraconazole, posaconazole, voriconazole and ketoconazole were <1 μg ml−1. M. furfur was more susceptible to itraconazole, terbinafine and bifonazole but tolerant to miconazole compared with M. globosa (P<0.05). Synergistic effects between terbinafine and itraconazole or between tacrolimus and itraconazole, ketoconazole or terbinafine occurred in 6, 7, 6 and 9 out of 37 strains, respectively. Phosphatases, lipases and proteases were mainly secreted in 51 isolates. Conclusions. Itraconazole, posaconazole, voriconazole and ketoconazole are theagents against which there is greatest susceptibility. Synergistic effects between terbinafine and itraconazole or tacrolimas and antifungals may be irrelevant to clinical application. Overproduction of lipases could enhance the skin inhabitation of M. furfur.

Regional Differences in the Permeability Barrier of the Skin—Implications in Acantholytic Skin Diseases

“…In addition, KLKs activate multiple enzymes involved in TJ degradation (e.g., PAR2, matrix metalloproteases) and may be at least partially responsible for TJ weakness in SGR and AGR regions [ 21 , 22 , 23 ]. Moreover, region-specific bacteria and fungi (Propionibacterium and Malassezia on SGR; Corynebacterium, Proteobacteria, and Staphylococcus aureus on AGR skin [ 2 , 17 ]) influence the permeability barrier by producing exogenous serine and cysteine peptidases [ 24 , 25 , 26 , 27 , 28 , 29 , 30 ].…”

Prevalence of Malassezia species on the skin of HIV-seropositive patients

“…In the nasolabial area, M. globosa (14%) was dominant, but three-fourths of the participants showed no growth of Malassezia 48 . Skin scraping analysis (culture method) showed that M. furfur (85%) and M. globosa (10%) were dominant in the thorax of 222 healthy Chinese subjects 49 .…”

Malassezia globosa Activates NLRP3 Inflammasome in Human Sebocytes

“…Similarly, preincubation with cytochalasin D or EDTA suppressed NLRP3 inflammasome activation and IL-1β release in this study, suggesting that yeast phagocytosis or M. globosa-derived proteases, at least metalloproteases, could be active in NLRP3 inflammasome activation of SZ95 sebocytes. Malasseziasecreted lipases, phospholipases and proteases may be important in pathogenicity and J o u r n a l P r e -p r o o f environmental adaption (Li et al, 2020). Since sebocytes express proteinase activated receptor 2 , the role of other M. globosa-derived proteases in NLRP3 inflammasome remains to be further studied.…”