Author Correction:Single human B cell-derived monoclonal anti-Candida antibodies enhance phagocytosis and protect against disseminated candidiasis

We thank the BBSRC, SULSA BioSKAPE and Pfizer Inc. for funding for a studentship for F.M.R. and the Wellcome Trust (086827, 075470, 099215, 099197 and 101873) and a Wellcome Trust ISSF award (105625), MRC CiC (MC_PC_14114) and MRC Centre for Medical Mycology and University of Aberdeen for funding and a Wellcome Trust Strategic Award (097377) and a Wellcome Trust grant 099197MA to T.F. and FCT Investigator IF/00033/2012 and PTDC/QUI-QUI/112537/2009 to A.S.P. We thank Ian Broadbent, Angus McDonald and Ron Gladue for constructive discussions; Chris Boston and Amanda Fitzgerald for advice on antibody expression and purification; Ed Lavallie and Wayne Stochaj for design and expression of the recombinant Hyr1; Louise Walker for high-pressure freezing of samples for TEM analysis; Jeanette Wagener for endotoxin testing of mAbs for in vivo experiments; Yan Liu of the Glycosciences laboratory for insight in the analysis with N-glycan array; Rebecca Hall and Mark Gresnigt for providing fungal strains; Andrew Limper and Theodore J. Kottom for providing Pneumocystis infected lung tissue extracts; David Williams for C. albicans mannoprotein; Christopher Thornton for A. fumigatus mannoprotein; Katie J. Doores for mAb PGT 128; and Gordon Brown for the murine Fc-Dectin-1. We are grateful to Lucinda Wight, Debbie Wilkinson and Kevin MacKenzie in the Microscopy and Histology Core Facility (Aberdeen University) and Raif Yuecel in the Iain Fraser Cytometry Centre (Aberdeen University) for their expert help with microscopy and cytometry experiments. We are also grateful to the staff at the University of Aberdeen Medical Research Facility for assistance with in vivo experiments and members of the Glycosciences Laboratory for their support of the Carbohydrate Microarray Facility. 18 January 2019 - Author Correction: Single human B cell-derived monoclonal anti-Candida antibodies enhance phagocytosis and protect against disseminated candidiasis F. M. Rudkin, I. Raziunaite, H. Workman, S. Essono, R. Belmonte, D. M. MacCallum, E. M. Johnson, L. Silva, A. S. Palma, T. Feizi, A. Jensen, L. P. Erwig & N. A. R. Gow Nature Communicationsvolume 10, Article number: 394 (2019)Peer reviewedPublisher PD

Butenafine

Nessun

Micafungin

Nessun

Antifungal agents

Antifungal drugs used to treat serious fungal disease fall primarily into three drug classes. These classes include the azoles, echinocandins, and polyenes. Both azoles and polyenes target the cell membrane while echinocandins specifically target cell-wall synthesis. Amphotericin B is the primary drug in the polyene arsenal and is considered fungicidal, or capable of killing fungi. Remaining drugs are primarily fungistatic, meaning that they function by inhibiting growth and viability to assist the patient's natural immunity in clearing infection. This chapter details drugs' mechanism of action, spectrum of activity, pharmacokinetics, and previously reported adverse events. In addition to drug characteristics and use, detection of resistance is discussed. Significant changes have been made in the interpretation of susceptibility testing results. Previously, break points were provided for all Candida spp., in general, but this has progressed to species-specific break points that are dependent on both the fungal species being tested and the drug under evaluation. In addition to making the break points species specific, the Clinical and Laboratory Standards Institute (CLSI) committee realized that the early break points were likely set too high. Current break points are approximately twofold lower than those previously published. Information regarding detecting resistance and incidence of resistance is discussed in regard to several clinically significant species