Abstract
The landscape of clinical mycology is constantly changing. New therapies for malignant and autoimmune diseases have led to new risk factors for unusual mycoses. Invasive candidiasis is increasingly caused by non-albicans Candida spp., including C. auris, a multidrug-resistant yeast with the potential for nosocomial transmission that has rapidly spread globally. The use of mould-active antifungal prophylaxis in patients with cancer or transplantation has decreased the incidence of invasive fungal disease, but shifted the balance of mould disease in these patients to those from non-fumigatus Aspergillus species, Mucorales, and Scedosporium/Lomentospora spp. The agricultural application of triazole pesticides has driven an emergence of azole-resistant A. fumigatus in environmental and clinical isolates. The widespread use of topical antifungals with corticosteroids in India has resulted in Trichophyton mentagrophytes causing recalcitrant dermatophytosis. New dimorphic fungal pathogens have emerged, including Emergomyces, which cause disseminated mycoses globally, primarily in HIV infected patients, and Blastomyces helicus and B. percursus, causes of atypical blastomycosis in western parts of North America and in Africa, respectively. In North America, regions of geographic risk for coccidioidomycosis, histoplasmosis, and blastomycosis have expanded, possibly related to climate change. In Brazil, zoonotic sporotrichosis caused by Sporothrix brasiliensis has emerged as an important disease of felines and people.
Highlights
In clinical mycology, as in other facets of healthcare, the only thing constant is change
This species is attributable for 15% of cases of candidemia in the United States [12], 20% in Russia [15], and rivals C. albicans as the leading cause of invasive disease in South Africa [16]
Among the most common cyp51A mutations conferring azole resistance is TR34 /L98H—a 34-bp tandem repeat in the gene’s promoter region with an associated substitution of lysine to histidine at codon 98, which results in an eight-fold upregulation of lanosterol 14α-demethylase [42,43]
Summary
As in other facets of healthcare, the only thing constant is change. Medical advances have improved and prolonged lives, but have increased the pool of individuals vulnerable to fungal disease; among these, new therapies for old diseases—such as monoclonal antibodies for autoimmune disease and small-molecule inhibitors (e.g. receptor tyrosine kinase inhibitors like ibrutinib) for B-cell malignancies—have resulted in reports of atypical and unusually severe fungal infections [1]. Decades of prolonged antifungal and antibacterial use in agriculture and medicine have altered the global microbiome, with a consequence being the emergence of drug-resistant fungal infections of plants, animals, and humans [3]. Within these contexts, changing trends are explored in global epidemiology of human fungal infections
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