| Fonsecaea pedrosoi | |
|---|---|
 | |
| Conidiophores ofFonsecaea pedrosoi from slide culture on Modified Leonian's agar | |
Scientific classification | |
| Domain: | Eukaryota |
| Kingdom: | Fungi |
| Division: | Ascomycota |
| Class: | Eurotiomycetes |
| Order: | Chaetothyriales |
| Family: | Herpotrichiellaceae |
| Genus: | Fonsecaea |
| Species: | F. pedrosoi |
| Binomial name | |
| Fonsecaea pedrosoi | |
| Synonyms | |
| |
Fonsecaea pedrosoi is a fungal species in the familyHerpotrichiellaceae, and the major causative agent ofchromoblastomycosis.[1] This species is commonly found in tropical and sub-tropical regions, especially in South America, where it grows as a soilsaprotroph.[2] Farming activities in theendemic zone are arisk factor for the development of chromoblastomycosis.[2][3]
Fonsecaea is a genus ofascomycetous fungi affiliated with the familyHerpotrichiellaceae.[4] The genus comprises three sibling species, all with pathogenic potential:F. pedrosoi,F. monophora andF. nubica.[4] The species was firstformally described in 1922 asHormodendrum pedrosoi by French parasitologistÉmile Brumpt.[5]Pablo Negroni transferred it to the genusFonsecaea in 1936.
Sparingly branched, brownishconidiophores produce clusters of one-celled, club-shaped conidia in short, dry, unbranched chains. APhialophora-like asexual state sometimes appears along with yeast cells at low pH.[6]
Fonsecaea pedrosoi occurs in soil and on plants and trees where it grows as asaprotroph.[4][3][7] It is found predominantly in tropical regions especially South- and Central America.[4][8] All three recognized species ofFonsecaea exhibit geographically patterned genetic variation. The closely related speciesF. monophora andF. nubica are distributed worldwide and show the greater population-levelgenetic diversity than the geographically restrictedF. pedrosoi.[4] Environmental surveys have documented the recovery ofF. pedrosoi on rotting wood of the Cambara tree (Gochnatia polymorpha) from theBrazilian Corporation of Agricultural Research forest inColombo, Paraná, Brazil.[9] It has also been isolated from living trees, stumps, woodpiles and fence posts in centralNigeria.[10]
Clinical isolates of grow consistently at temperatures up to 35 °C (95 °F).[11] In contrast, environmental isolates ofF. pedrosoi exhibit growth consistently up to 35 °C, and irregularly up to 37 °C (99 °F)[12] Physiological studies have shown the degradation ofurea andtyrosine, and the lack of growth on the proteinsgelatin,casein and thepurinesxanthine andhypoxanthine.[12] Likewise,lipase activity was demonstrated, butphospholipase,collagenase andamylase were not expressed.[12]
Fonsecaea pedrosoi is one of several main causative agents of humanchromoblastomycosis, achronic fungal infection localized to skin andsubcutaneous tissue.[1][8][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 asconidia or hyphal fragments.[1] Once introduced in the subcutaneous tissues, thepropagules germinate to establish an invasivemycelium associated withsclerotic cells.[1] This proliferation manifests as a well-defined, chronically progressive, crustedulceration of the skin known as chromoblastomycosis.[3][2][13] Clinically it is often misdiagnosed assquamous cell carcinoma.[2]
The disease is characterized by the appearance of spherical, brownish yellow cells with thick, darkly pigmented walls.[14] The presence of the agent is associated with host cell proliferation and enlargement known ashyperplasia localized to thestratified squamous epithelium and the formation of mycoticgranulomas.[2] Sclerotic bodies are present both extracellularly and intracellularly throughout the affected tissue and are a defining feature of chromoblastomycosis.[2][13] The melanin content of sclerotic bodies may be important in the establishment of host immune responses.[1]
Farmers in Central and South America are most susceptible to chromoblastomycosis due toF. pedrosoi.[13][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,[13] while Japanese infections have shown evenly distributed infection rates between the sexes.[13]
Infections byF. pedrosoi are more difficult to treat than those ofF. monophora.[8] In severe cases, treatment is quite complex and involves a combination of antifungal drug therapy and surgical excision.[3] Antifungal agents likeitraconazole andterbinafine are commonly used. Surgery is often used to treat small, localized infections,[2] althoughcryotherapy has been suggested an alternative approach.[3] Topical application ofamphotericin B followed by long-term administration of oral antifungal therapy has been shown to be effective in the treatment of corneal chromoblastomycosis fromF. pedrosoi.[7] The diagnosis and treatment of chromoblastomycosis byF. 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.[13][8]
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