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Fungal Infections and Studies · Journal article
Frontiers in Bioscience-landmark · August 21, 2026
A consensus or society position rather than new primary data.
This is a narrative review summarizing the molecular basis of fungal esophagitis, shifting epidemiology toward immunocompromised non-HIV populations, and emerging antifungal resistance mechanisms. It identifies rezafungin, ibrexafungerp, and fosmanogepix as promising alternatives to fluconazole for refractory disease, but does not present clinical trial outcomes or comparative efficacy data.
Journal article. Patients with fungal esophagitis, predominantly Candida species; historically HIV-infected patients; increasingly immunocompromised populations including oncology patients on immune checkpoint inhibitors, eosinophilic esophagitis patients on oral corticosteroids, and solid-organ transplant recipients..
Fungal esophagitis epidemiology has shifted from HIV infection toward oncology patients on immune checkpoint inhibitors, eosinophilic esophagitis patients on oral corticosteroids, and solid-organ transplant recipients. Pathogenic mechanisms include adhesion, hyphal transition, biofilm formation, and mucosal immune dysfunction involving impaired T helper 17/interleukin 17 signaling and reduced antimicrobial peptide activity. Antifungal resistance driven by efflux pump overexpression, ERG11 mutations conferring azole resistance, and FKS gene mutations leading to reduced echinocandin susceptibility.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
This review guides clinicians to recognize shifting epidemiology and emerging resistance patterns in fungal esophagitis, and to consider novel antifungal agents (rezafungin, ibrexafungerp, fosmanogepix) for refractory cases. However, specific efficacy, safety, or comparative outcome data are not provided to inform treatment decisions at the individual patient level.
A narrative review synthesizing molecular pathogenesis, epidemiology, and treatment strategies for fungal esophagitis, offering expert perspective on emerging resistance and novel agents without reporting primary clinical trial data.
This review guides clinicians to recognize shifting epidemiology and emerging resistance patterns in fungal esophagitis, and to consider novel antifungal agents (rezafungin, ibrexafungerp, fosmanogepix) for refractory cases. However, specific efficacy, safety, or comparative outcome data are not provided to inform treatment decisions at the individual patient level.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
Fungal esophagitis, predominantly caused by Candida species, remains the leading form of infectious esophagitis worldwide. Although historically linked to human immunodeficiency virus infection, its epidemiology has shifted over recent decades, with a growing incidence among oncology patients receiving immune checkpoint inhibitors, individuals with eosinophilic esophagitis on oral corticosteroids, and solid-organ transplant recipients. Increasing evidence highlights that disease pathogenesis extends beyond simple fungal overgrowth and involves intricate host–pathogen interactions. Pathogenic mechanisms such as adhesion, hyphal transition, and biofilm formation enhance fungal virulence, while mucosal immune dysfunction, particularly impaired T helper 17/interleukin 17 signaling and reduced antimicrobial peptide activity, predisposes to persistent infection. Antifungal resistance represents an emerging challenge, driven by efflux pump overexpression, ERG11 mutations conferring azole resistance, and mutations of FKS genes leading to reduced echinocandin susceptibility. These molecular mechanisms underscore the complexity of treatment and have important implications for antifungal selection and clinical management. While fluconazole remains the first-line agent for most cases, the increasing prevalence of non-albicans Candida species and drug resistance underscore the importance of alternative medications with different molecular targets. Agents such as the recently approved rezafungin as well as compounds such as ibrexafungerp and fosmanogepix, represent promising options for the treatment of refractory disease. This review synthesizes current advances in the molecular pathogenesis of fungal esophagitis, with particular emphasis on host–fungal interactions, antifungal resistance mechanisms, and novel treatment strategies. A deeper understanding of these processes is essential to improve management and to guide the development of innovative immunomodulatory and antifungal therapies.
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