Abstract
Exposure to fungal pathogens from the environment is inevitable and with the number of at-risk populations increasing, the prevalence of invasive fungal infection is on the rise. An interesting group of fungal organisms known as thermally dimorphic fungi predominantly infects immunocompromised individuals. These potential pathogens are intriguing in that they survive in the environment in one form, mycelial phase, but when entering the host, they are triggered by the change in temperature to switch to a new pathogenic form. Considering the growing prevalence of infection and the need for improved diagnostic and treatment approaches, studies identifying key components of fungal recognition and the innate immune response to these pathogens will significantly contribute to our understanding of disease progression. This review focuses on key endemic dimorphic fungal pathogens that significantly contribute to disease, including Histoplasma, Coccidioides and Talaromyces species. We briefly describe their prevalence, route of infection and clinical presentation. Importantly, we have reviewed the major fungal cell wall components of these dimorphic fungi, the host pattern recognition receptors responsible for recognition and important innate immune responses supporting adaptive immunity and fungal clearance or the failure thereof.
Highlights
Dimorphic fungi produce conidia that are responsible for geographical dispersal and host infection
Without Sod3, an extracellular superoxide dismutase (SOD) produced during infection, H. capsulatum cannot survive in activated macrophages
The importance of understanding how our immune system interacts with these dimorphic fungal pathogens will provide critical insight into potential vaccine development and therapeutic interventions
Summary
Fungi can be found in almost every environment on earth and are abundant in organic substrates such as soil and plant debris. Dimorphic fungi produce conidia that are responsible for geographical dispersal and host infection It is the transition into yeast form that drives pathogenicity, as these organisms have evolved to alter their cell wall components and proteins to survive at mammalian body temperature and evade immune responses. The main thermally dimorphic pathogens of humans are globally distributed and include Histoplasma capsulatum, Blastomyces dermatiditis, Coccidioides immitis/posadasii, Paracoccidioides brasiliensis/lutzii, Talaromyces marneffei (formerly known as Penicillium marneffei), Sporothrix schenckii and newly identified, Emergomyces spp. These organisms are primary pathogens, but for this review, we will focus on key pathogens that cause the most infections, including, Histoplasma Coccidioides and Talaromyces spp
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