
A Model for Trans-Kingdom Pathogenicity in Fonsecaea Agents of Human Chromoblastomycosis
2018; Frontiers Media; Volume: 9; Linguagem: Inglês
10.3389/fmicb.2018.02211
ISSN1664-302X
AutoresGheniffer Fornari, Renata Rodrigues Gomes, Juliana Degenhardt-Goldbach, Suelen Silvana dos Santos, Sandro Rogério de Almeida, Germana Dávila dos Santos, Marisol Dominguez Muro, Cleusa Bona, Rosana Hermínia Scola, Edvaldo da Silva Trindade, Israel Henrique Bini, Lisandra Santos Ferreira-Maba, Daiane Rigoni Kestring, Mariana Machado Fidelis do Nascimento, Bruna Jacomel Favoreto de Souza Lima, Morgana Ferreira Voidaleski, Douglas André Steinmacher, Bruna da Silva Soley, Shuwen Deng, Anamélia Lorenzetti Bocca, Moisés Batista da Silva, Cláudio Guedes Salgado, Conceição Maria Pedroso e Silva de Azevedo, Vânia Aparecida Vicente, Sybren de Hoog,
Tópico(s)Antifungal resistance and susceptibility
ResumoThe fungal genus Fonsecaea comprises etiological agents of human chromoblastomycosis, a chronic implantation skin disease. The current hypothesis is that patients acquire the infection through an injury from plant material. The present study aimed to evaluate a model of infection in plant and animal hosts to understand the parameters of trans-kingdom pathogenicity. Clinical strains of causative agents of chromoblastomycosis (Fonsecaea pedrosoi and Fonsecaea monophora) were compared with a strain of Fonsecaea erecta isolated from a living plant. The clinical strains of F. monophora and F. pedrosoi remained concentrated near the epidermis, whereas F. erecta colonized deeper plant tissues, resembling an endophytic behavior. In an invertebrate infection model with larvae of a beetle, Tenebrio molitor, F. erecta exhibited the lowest survival rates. However, F. pedrosoi produced dark, spherical to ovoidal cells that resembled muriform cells, the invasive form of human chromoblastomycosis confirming the role of muriform cells as a pathogenic adaptation in animal tissues. An immunologic assay in BALB/c mice demonstrated the high virulence of saprobic species in animal models was subsequently controlled via host higher immune response.
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