Virulence factors of Malassezia strains isolated from pityriasis versicolor patients and healthy individuals

Over the last decade, Malassezia species have emerged as increasingly important pathogens associated with a wide range of dermatological disorders and bloodstream infections. The pathogenesis of Malassezia yeasts is not completely clear, but it seems to be strictly related to Malassezia strains and hosts and needs to be better investigated. This study aimed to assess the enzymatic activities, biofilm formation and in vitro antifungal profiles of Malassezia spp. from pityriasis versicolor (PV) and healthy patients. The potential relationship between virulence attributes, the antifungal profiles and the origin of strains was also assessed. A total of 44 Malassezia strains isolated from patients with (n = 31) and without (n = 13) PV were employed to evaluate phospholipase (Pz), lipase (Lz), and hemolytic (Hz) activities and biofilm formation. In addition, in vitro antifungal susceptibility testing was conducted using the CLSI broth microdilution with some modifications. A high percentage of strains produced Pz, Lz, Hz and biofilm regardless of their clinical origin. The highest number of strains producing high enzymatic activities came from PV patients. A correlation between the intensity of hydrolytic activities (Lz and Pz activities) and the Hz activity was detected. Positive associations between Lz and the low fluconazole susceptibility and Hz and biofilm formation were observed. These results suggest that enzyme patterns and biofilm formation along with antifungal profiles inter-play a role in the pathogenicity of Malassezia spp. and might explain the implication of some Malassezia spp. in invasive fungal infections and in the development of inflammation. LAY SUMMARY: There is still little information on the virulence factors of Malassezia spp., despite their implication in severe diseases. Phospholipase, lipase, and hemolytic activities, biofilm formation and decreased antifungal susceptibility seem to contribute to their virulence in susceptible hosts

Prevention and Immunotherapy of Secondary Murine Alveolar Echinococcosis Employing Recombinant EmP29 Antigen

Alveolar echinococcosis (AE) is caused by infection with the larval stage of the tapeworm Echinococcus multilocularis. An increasing understanding of immunological events that account for the metacestode survival in human and murine AE infection prompted us to undertake explorative experiments tackling the potential of novel preventive and/or immunotherapeutic measures. In this study, the immunoprotective and immunotherapeutic ability of recombinant EmP29 antigen (rEmP29) was assessed in mice that were intraperitoneally infected with E. multilocularis metacestodes. For vaccination, three intraperitoneal injections with 20μg rEmP29 emulsified in saponin adjuvants were applied over 6 weeks. 2 weeks after the last boost, mice were infected, and at 90 days post-infection, rEmP29-vaccinated mice exhibited a median parasite weight that was reduced by 75% and 59% when compared to NaCl- or saponin-treated control mice, respectively. For immunotherapeutical application, the rEmP29 (20μg) vaccine was administered to experimentally infected mice, starting at 1 month post-infection, three times with 2 weeks intervals. Mice undergoing rEmP29 immunotherapy exhibited a median parasite load that was reduced by 53% and 49% when compared to NaCl- and saponin-treated control mice, respectively. Upon analysis of spleen cells, both, vaccination and treatment with rEmP29, resulted in low ratios of Th2/Th1 (IL-4/IFN-γ) cytokine mRNA and low levels of mRNA coding for IL-10 and IL-2. These results suggest that reduction of the immunosuppressive environment takes place in vaccinated as well as immunotreated mice, and a shift towards a Th1 type of immune response may be responsible for the observed increased restriction of parasite growth. The present study provides the first evidence that active immunotherapy may present a sustainable route for the control of AE

Potentiation effect of the AMPK activator A-769662 on cardiac myocytes metabolism and survival

Abstract 286 van Poster session 2 Frontiers in CardioVascular Biology, London 30th March – 1st April 2012 Second Congress of the ESC Council on Basic Cardiovascular Science