Chromoblastomycosis is a chronic subcutaneous mycotic infection caused by pigmented or dematiaceous saprophytic moulds ubiquitous in the environment. The most common etiologic agents are Fonsecaea pedrosoi and Cladophialophora carrionii, both of which can be isolated from plant debris. The infection usually follows traumatic inoculation through penetrating thorn or splinter wounds. The fungal agents develop as small clusters of cells known as muriform bodies. Several months after the injury, painless papules or nodules appear in the affected area progressing to scaly and verrucose plaques. Direct examinations of skin scrapings or histopathologic study demonstrates the typical muriform bodies. Microbiologic culture is necessary for the correct determination of the etiologic agent. Itraconazole is the treatment of choice, often in combination with surgery. Even so, results are often unsatisfactory as patients present late to medical services because of lack of funds and the fact that the disease usually affects the main family earner.
"The genus Fonsecaea comprises etiologic agents of human chromoblastomycosis, a chronic (sub)cutaneous infection eventually leading to cauliflower-like eruptions on the skin , . The fungus is present in human tissue in the form of muriform cells. "
[Show abstract][Hide abstract] ABSTRACT: Members of the fungal genus Fonsecaea causing human chromoblastomycosis show substantial geographic structuring. Genetic identity of clinical and environmental strains suggests transmission from plant debris, while the evolutionary processes that have led to spatially separated populations have remained unexplained. Sequences of ITS, BT2, ACT1, Cdc42, Lac and HmgA were analyzed, either by direct sequencing or by cloning. Thirty-seven clinical and environmental Fonsecaea strains from Central and South America, Asia, Africa and Europe were sequenced and possible recombination events were calculated. Phylogenetic trees of Cdc42, Lac and HmgA were statistically supported, but ITS, BT2 and ACT1 trees were not. The Standardized Index of Association (I(A) (S)) did not detect recombination (I(A) (S) = 0.4778), neither did the Phi-test for separate genes. In Fonsecaea nubica non-synonymous mutations causing functional changes were observed in Lac gene, even though no selection pressures were detected with the neutrality test (Tajima D test, p>0.05). Genetic differentiation of populations for each gene showed separation of American, African and Asian populations. Strains of clinical vs. environmental origin showed genetic distances that were comparable or lower than found in geographic differentiation. In conclusion, here we demonstrated clonality of sibling species using multilocus data, geographic structuring of populations, and a low functional and structural selective constraint during evolution of the genus Fonsecaea.
PLoS ONE 08/2012; 7(8):e41512. DOI:10.1371/journal.pone.0041512 · 3.23 Impact Factor
"The initial treatment consisted of excision, skin grafting and other treatments, such as localized hyperthermia and cryosurgery or administering itraconazole, 5-fluorocytosine, or amphotericin B1-3. Effective treatments usually try to prevent the localized recurrence by wide margin excision of small or localized lesion areas. "
[Show abstract][Hide abstract] ABSTRACT: We report herein a case of chromoblastomycosis caused by Fonsecaea (F.) pedrosoi in a 39-year-old male, who showed multiple, asymptomatic, scaly erythematous plaques on the left shin for 12 months. Histopathologically, chronic granulomatous inflammation and either sclerotic or muriform cells were observed. The fungal culture produced typical black colonies of F. pedrosoi. The DNA sequence of the internal transcribed spacer (ITS) region of the clinical sample was 100% match to that of F. pedrosoi IFM 47061 (GenBank accession number AB240943). The patient was treated with 200 mg of itraconazole daily, for 3 months. Skin lesions were improved. In Korea, only 9 cases of chromoblastomycosis, including this case, have been reported until now. The etiologic agent was F. pedrosoi in the majority of cases (6/9;67%). The incidence of chromoblastomycosis was slightly higher in female, and the upper limbs were more affected than the lower limbs in patients.
Annals of Dermatology 08/2011; 23(3):369-74. DOI:10.5021/ad.2011.23.3.369 · 1.39 Impact Factor
"F. pedrosoi is usually limited to skin tissue, most commonly on the lower limbs. Infection usually occurs after exposure to the fungus via contaminated soil, splinters or sharp farm equipment, and results in long-term inflammation, suppurative granulomatous dermatitis and fibrosis [1,2]. The affected patients are typically low-income workers that engage in agricultural or manual labour in tropical and subtropical countries. "
[Show abstract][Hide abstract] ABSTRACT: The pathogenic fungus Fonsecaea pedrosoi constitutively produces the pigment melanin, an important virulence factor in fungi. Melanin is incorporated in the cell wall structure and provides chemical and physical protection for the fungus.We evaluated the production of nitric oxide (NO) in macrophages, the oxidative burst and the inducible nitric oxide synthase (i-NOS) activity in interactions between activated murine macrophages and F. pedrosoi. Experiments were carried out with or without tricyclazole (TC) treatment, a selective inhibitor of the dihydroxynaphthalene (DHN)-melanin biosynthesis pathway in F. pedrosoi. The paramagnetisms of melanin and the TC-melanin were analysed by electron spin resonance. The fungal growth responses to H2O2 and to S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide donor, were also evaluated.
Melanised F. pedrosoi cells were more resistant to both H2O2 and NO. Nitrite was not detected in the supernatant of macrophages incubated with melanised fungal cells. However, i-NOS expression was unaffected by the presence of either untreated control F. pedrosoi or TC-treated F. pedrosoi. In addition, the inhibition of the DHN-melanin pathway by TC improved the oxidative burst capability of the macrophages.
The NO-trapping ability of F. pedrosoi melanin is an important mechanism to escape the oxidative burst of macrophages.
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