User:Tingsonn/sandbox
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| Conidiophores of Fonsecaea pedrosoi from slide culture on Modified Leonian's agar. | |
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| Species: | F. pedrosoi
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| Binomial name | |
| Fonsecaea pedrosoi (Brumpt) Negroni (1936)
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Hormodendrum pedrosoi Brumpt (1922) | |
Fonsecaea pedrosoi is the major causative agent of chromoblastomycosis.[1] This species is commonly found in tropical and sub-tropical regions where it grows as a soil saprotroph.[2] Farming activities in the endemic zone are a risk factor for the development of chromoblastomycosis.[2][3]
Classification[edit]
Fonsecaea is a genus of ascomycetous fungi affiliated with the family Herpotrichiellaceae.[4] The genus comprises three sibling species. all with pathogenic potential: F. pedrosoi, F. monophora and F. nubica.[4]
Ecology and distribution[edit]
Fonsecaea pedrosoi occurs in soil and on plants and trees where it grows as a saprotroph.[4][3][5] It is found predominantly in tropical regions especially South- and Central America.[4][6] All three species of Fonsecaea exhibit geographically patterned genetic variation. The closely-related species F. monophora and F. nubica are distributed worldwide and show the greater population-level genetic diversity than the geographically restricted F. pedrosoi.[4]
Human disease[edit]
Fonsecaea pedrosoi is one of several main causative agents of human chromoblastomycosis, a chronic fungal infection localized to skin and subcutaneous tissue.[1][6][2] The disease was first described by Alexandrino Pedroso in 1911.[2] The fungus infects the host through the traumatic implantation of sexual spores known as conidia or hyphal fragments.[1] Once introduced in the subcutaneous tissues, the propagules germinate to establish an invasive mycelium associated with sclerotic cells.[1] This proliferation manifests as a well-defined, chronically progressive, crusted ulceration of the skin known as chromoblastomycosis.[3][2] [7] It is often misdiagnosed as squamous cell carcinoma.[2] The presence of pigmented, sclerotic bodies within these lesions is a defining feature of chromoblastomycosis.[2]
Histology[edit]
Chromoblastomycosis is characterized by the appearance of spherical, brownish yellow cells with thick, darkly pigmented walls.[1] The presence of the agent is associated with host cell proliferation and enlargement known as hyperplasia localized to the stratified squamous epithelium and the formation of mycotic granulomass.[2] Sclerotic bodies are present both extracellularly and intracellularly throughout the affected tissue.[2][7]
Treatment[edit]
Infections by F.pedrosoi are more difficult to treat than those of F. monophora.[6] In severe cases, treatment is quite complex and involves a combination of antifungal drug therapy and surgical excision.[3] Antifungal agents like itraconazole and terbinafine are commonly used. Surgery is often used to treat small, localized infections,[2] although cryotherapy has been suggested an alternative approach.[3] Topical application of amphotericin B followed by long-term administration of oral antifungal therapy has been shown to be effective in the treatment of corneal chromoblastomycosis from F. pedrosoi.[5] The diagnosis and treatment of chromoblastomycosis by F.pedrosoi remains clinically challenging due to the relative rarity of the disease, its slow, chronic nature, the absence of clinical features readily differentiating it from other more common diseases such as squamous cell carcinoma, the restricted nature of therapies, and the lack of literature.[7][6]
Risk factors for disease[edit]
Farmers in Central and South America are most susceptible to chromoblastomycosis due to F. pedrosoi.[7][3] Infection often occurs in the upper body and legs of agricultural laborers since these areas are more prone to exposure to infected soil, plant debris or other fomites.[3] The sex ratio of disease is globally variable. In Brazil, the agent has shown a 4:1 proclivity for men, likely as a function of exposure differences relating to work and lifestyle,[7] while Japanese infections have shown evenly distributed infection rates between the sexes.[7]
References[edit]
- ^ a b c d e Alviano, D; Franzen, A; Travassos, L; Holandino, C; Rozental, S; Ejzemberg, R; Rodrigues, M. "Melanin from Fonsecaea pedrosoi Induces Production of Human Antifungal Antibodies and Enhances the Antimicrobial Efficacy of Phagocytes". Infect Immun 2004. 72 (1): 229–237. doi:10.1128/IAI.72.1.229-237.2004.
- ^ a b c d e f g h i j Deb Roy, A; Das, D; Deka, M. "Chromoblastomycosis – A clinical mimic of squamous carcinoma". Mycopathologia 2013. 6 (9): 458–460. doi:10.4066/AMJ.2013.1806.
- ^ a b c d e f g Nimrichter, L; Cerqueira, M; Leitao, E; Miranda, K; Nakayasu, E; Almeida, S; Rodrigues, M. "Structure, Cellular Distribution, Antigenicity, and Biological Functions of Fonsecaea pedrosoi Ceramide Monohexosides". Infection and Immunity 2005. 73 (12): 7860–7868. doi:10.1128/IAI.73.12.7860-7868.2005.
{{cite journal}}: Cite has empty unknown parameter:|1=(help) - ^ a b c d e Najafzadeh, M; Sun, J; Vincete, V; Klaassen, C; Bonifaz, A; Gerrits van den Ende, A; Sybren de Hoog, G. "Molecular Epidemiology of Fonsecaea Species". Emerging Infectious Diseases 2011. 17 (3): 464–69. doi:10.3201/eid1703.100555.
{{cite journal}}: Cite has empty unknown parameter:|1=(help) - ^ a b Sangwan, Jyoti; Jachuck, SJ (2013). "Fonsecaea Pedrosoi: A Rare Etiology in Fungal Keratitis". JOURNAL OF CLINICAL AND DIAGNOSTIC RESEARCH. doi:10.7860/JCDR/2013/6627.3491.
- ^ a b c d Yang, Y; Yongxuan, H; Zhang, J; Li, X; Lu, C; Xi, L. "A refractory case of chromoblastomycosis due to Fonsecaea monophora with improvement by photodynamic therapy". Medical Mycology 2012. 50 (1): ), 649–653. doi:10.3109/13693786.2012.655258.
- ^ a b c d e f Kondo, M; Hiruma, M; Nishioka, Y; Mochida, K; Ikeda, S; Ogawa, H. "A case of chromomycosis caused by Fonsecaea pedrosoi and a review of reported cases of dematiaceous fungal infection in Japan". Blackwell Publishing Ltd 2005. 48 (1): 221–225. doi:10.1111/j.1439-0507.2005.01089.x.
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