An Autochthonous Phaeohyphomycotic Nail Infection in Canada Caused by Hendersonula toruloidea

Abstract

A case of an autochthonous toenail infection caused by Hendersonula toruloidea is presented. H. toruloidea was characterized by thick, branching septate brown-walled hyphae of a non-dermatophyte in microscopic tissue mounts in 25% Na0H with 5% glycerol. Cultures grew out on Littman's agar and Sabouraud peptone glucose agar plus chloramphenicol, but only if cycloheximide was not present. In vitro, the H. toruloidea isolate was characterized by copious 1-to 2-celled hyaline to dark-brown arthroconidia deriving from the fragmentation of aerial hyphae. It is likely that more infections due to H. toruloidea will be diagnosed if cycloheximide-free media are routinely used in the isolation of organisms from suspected dermatophyte infections.

Scytalidium dimidiatum and Lecythophora hoffmannii: unusual causes of fungal infections in a patient with AIDS

“…In temperate zones infections generally occur in immigrants from areas of endemicity. Kane et al (7) described the first indigenous Canadian case in 1990, and Frankel and Rippon reported three cases of dermatomycosis in the temperate regions of the United States (4). There has been only one report of a case in Australia (10) in which S. hyalinum was isolated from the toenail of a patient with chronic onychomycosis.…”

Invasive Nattrassia mangiferae infections: case report, literature review, and therapeutic and taxonomic appraisal

“…mangiferae and S. hyalinum, however, have a reputation for being very difficult to treat successfully not just when they are the cause of deep infections but also when they are the cause of cutaneous infections. Sporadic cures have been reported with clotrimazole (20), nail avulsion-ciclopirox olamine under occlusion (54), tioconazole (one of three patients only) (25), 10% boric acid in mineral oil (27), and apparently, Grow Strong nail hardener following clotrimazole therapy (one of three patients) (14). Ineffective results have been ascribed to ciclopirox olamine ϩ glutaraldehyde (54), clotrimazole (14,45), econazole (14), bifonazole (19), tioconazole (25), miconazole (14), ketoconazole (14,22,45), itraconazole (24), half- strength Whitfield's ointment (31), griseofulvin (19), and in one patient, a succession of various topical antifungal preparations (19).…”

“…As the chlamydospores develop and become melanized, the colonies darken from off-white to yellowish grey, grey, or black, depending on their abundance. Their development can be influenced by medium, forming less abundantly on phytone yeast extract agar (BBL) than on Pablum cereal agar (27). Most isolates also produce a strong yellow, diffusible pigment.…”

“…Other papers documented the incidence of infection in residents of areas where the fungus was known to be endemic (20,21,30,31). In North America, the fungus is being seen with increasing frequency in the dermatological diagnostic laboratory (28,60), but relatively few cases of infection occur in individuals who have no history of residence or travel elsewhere (14,27), despite the cosmopolitan distribution of the fungus on various hosts, including Arbutus, Ficus, Citrus, Juglans, and others (11). Only rare reports of infection have been attributed to S. lignicola (7,8,13).…”

Chinese National Consensus Committee of Experts on Kawasaki Disease and Chinese Journal of Contemporary Pediatrics: The expert consensuses on Intravenous Immunoglobulin, aspirin, and Glucocorticoid

“…1 Chinese expert consensus on IVIG for KD [17] 1 .1 Mechanism of IVIG for the treatment of KD The main objectives of treatment in the acute phase of KD are to control and terminate the in ammatory response, reduce the incidence of coronary artery damage, and prevent coronary thrombosis [23].IVIG is an immunoglobulin preparation isolated from the blood of healthy people, of which IgG is the most abundant immunoglobulin, accounting for more than 95%. The IgG molecule is hydrolyzed to obtain a crystallizable fragment with an important role ( Fragment crystallizable (Fc), IgG Fc can bind to harmful complement components in the body and block their deposition in target tissues, thus avoiding immune damage, while IgG Fc can bind to Fc receptors and regulate immune function by activating intrinsic immunity [24,25]. Although the therapeutic regimen of IVIG applied to Kawasaki disease has been gradually re ned and matured, its speci c mechanism has not been elucidated in detail, and it is currently believed that IVIG treatment of Kawasaki disease may be through the following pathways:…”