Image_4_A Model for Trans-Kingdom Pathogenicity in Fonsecaea Agents of Human Chromoblastomycosis.TIF (9.98 MB)

Image_4_A Model for Trans-Kingdom Pathogenicity in Fonsecaea Agents of Human Chromoblastomycosis.TIF

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posted on 09.10.2018 by Gheniffer Fornari, Renata Rodrigues Gomes, Juliana Degenhardt-Goldbach, Suelen Silvana dos Santos, Sandro Rogério de Almeida, Germana Davila dos Santos, Marisol Dominguez Muro, Cleusa Bona, Rosana Herminia Scola, Edvaldo S. Trindade, Israel Henrique Bini, Lisandra Santos Ferreira-Maba, Daiane Rigoni Kestring, Mariana Machado Fidelis do Nascimento, Bruna Jacomel Favoreto de Souza Lima, Morgana F. Voidaleski, Douglas André Steinmacher, Bruna da Silva Soley, Shuwen Deng, Anamelia Lorenzetti Bocca, Moises B. da Silva, Claudio G. Salgado, Conceição Maria Pedroso e Silva de Azevedo, Vania Aparecida Vicente, Sybren de Hoog

The 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.