I’ve been reading quite a bit about antifungals lately and one of the things I realized is the many formulations of amphotericin. Actually, the realization I had was I didn’t know the differences between them. It is a polyene antifungal that has broad spectrum antifungal activity (including Leshmania spp) but it is limited by its
Category: Fungi
This post will not cover the clinical course or risk factors. We’ll be going over the direct fluorescence antibody, PCR, as well as the elusive beta-D glucan as well as taking a brief look at the original ways we used to diagnose PJP (or in some places, how they still diagnose it. In the days
This is the cell wall of fungi. It is not inert and, the cell wall undergoes a consistent process of assembly and remodeling during cell growth. Glucan is the most abundant polysaccharide, and it is made up of glucose polymers linked by carbon at the first and third position: Back in the day (roughly the
The ACTIVE trial! This is a phase III, RCT, double blind, multicenter, non-inferiority trial comparing isavuconazole vs caspofungin in invasive candidiasis. Folks, in ID, it doesn’t get any better than this (look at all these studies!) Exclusion criteria were Candida in any body part (i.e. osteomyelitis, IE, meningitis), severe immunodeficiency, >48hrs of other antifungal therapy.
Retrospective study from South Korea evaluating the predictive value of BD glucan in the age of mold active triazole prophylaxis. They recruited patients that underwent induction chemotherapy, SCT, or GVHD treatment that had BD glucans throughout their stay while on posa or micafungin prophylaxis. They defined a positive BD glucan as 2 or more BDG




