Species name and common name: Fonsecaea pedrosoi complex which includes F. monophora and the previously named species F. compacta, now. Fonsecaea pedrosoi (Brumpt) Negroni, Rev. Inst. Bact.: () [MB#]. Muriform cells, the parasitic form of Fonsecaea pedrosoi, are highly prevalent in infected tissues, especially in long-standing lesions. In this.

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Palmeira, Sonia Rozental, Lucimar F. Kneipp, Leonardo Nimrichter, Daniela S. Fonsecaea pedrosoi is the principal etiologic agent of chromoblastomycosis, a fungal disease whose pathogenic events are poorly understood. Treatment of the disease presents poor effectiveness and serious side effects.

The disease is epidemiologically important in several regions, which has stimulated studies focused on the biology and pathogenic potential of its major causative agent. In this review, we summarize the current knowledge on the biological aspects of F.

Fonsecaea pedrosoi – Wikipedia

Chromoblastomycosis or chromomycosis is a chronic fungal disease usually limited to the skin and subcutaneous tissues. Chromoblastomycosis is caused by a list of dematiaceous fungi sharing as a common feature the constitutive synthesis and deposition of melanin at fungal cell wall Rippon, ; De Hoog et al.

The mycosis begins with a transcutaneous trauma allowing hyphal fragments and conidial forms to penetrate. It occurs preferentially in humans, although some cases of chromoblastomycosis have been reported in other mammals McGinnis et al.

The etiologic agents of chromoblastomycosis are Fonsecaea pedrosoiFonsecaea compacta a morphological variety of F.

Recently, Exophiala jeanselmei and Exophiala spinifera have also been reported as agents of chromoblastomycosis Silva et al. Major sites of chromoblastomycosis occurrence include Brazil Silva et al. In Brazil, the Amazon region has been considered as the main chromoblastomycosis endemic area Silva et al. The infection generally affects individuals who are engaged in farming and males are more commonly affected c. The explanation for this predominance is not clear, but men are assumed to be more commonly involved in agricultural work and are more prone to inflict injuries on themselves, thereby causing self-inoculation.

Moreover, the possible inhibitory effect of female hormones on the fungal growth may partially explain the relatively low number of cases in women Hernandez-Hernandez et al. No racial predilection is reported. Patients with the disease are most commonly aged 30—50 years. A correlation with HLA-A29 antigen suggests that genetic factors may play a role as well Tsuneto et al. The sites most commonly affected are the lower extremities, especially the feet, which are more likely to be in contact with infected materials, soil and plants or rotting wood Rippon et al.

Hands, arms and the buttocks are also frequently involved, and sporadic reports mention lesions on the ears, cornea, neck, face, breasts, chest and abdomen Bittencourt et al.

Initial lesions of chromoblastomycosis are usually erythematous papules, which gradually enlarge to display varying morphologies such as verrucous nodules, cauliflower-like tumors and psoriasis-like plaques Richard-Blum et al.

In the later stages of infection, dissemination may occur by extension of the lesions as satellites along the lymph vessels or by autoinoculation through scratching Kondo et al.

Systemic invasion following chromoblastomycosis is very rare. However, the occurrence of F. These fungal forms are often seen in the deeper portions of the lesion, whereas hyphae and budding cells may be present at the surface of the lesions Bonifaz et al.

Sclerotic bodies may be found individualized, in clusters or within giant cells. For cultures, parts of the biopsy sample could be used for growth in Sabouraud-glucose agar supplemented with antibiotics. Small black colonies usually appear within 2 weeks. No serological procedures are available for the diagnosis of chromoblastomycosis. Recently, molecular approaches using the gene coding for ribosomal subunits were described as promising tools for dematiaceous fungi taxonomy Caligiorne et al.


Neutrophils and macrophages are key cells in tonsecae immune response against chromoblastomycosis. The typical granulomatous reaction observed in patients with the disease is regulated by polymorphonuclear neutrophils PMNs Uribe et al.

Macrophage-derived cytokine production pedosoi killing of F. The mechanisms of host defense in chromoblastomycosis have not been satisfactorily investigated. It remains unknown whether humoral immunity plays a significant role in fungal disease control, although antibodies with direct antimicrobial action have been detected in sera of infected individuals Alviano et al. Individuals from endemic areas with previous exposure to the fungus develop a specific humoral response, although it has not been clearly correlated with the course of the disease Esterre et al.

The period required for serological conversion is variable, and some patients may present positive serology for more than 1 year after the end of antifungal treatment Esterre et al. The role of cellular immunity in chromoblastomycosis has been more deeply investigated in the last years.

Delayed-type hypersensitivity reactions can be used to indicate T-cell-mediated inflammatory responses to either exogenous antigens or autoantigens Brown et al. This parameter is often used to evaluate the host cellular immune response to a wide range of pathogens, including F. There are few studies evaluating the immunophenotype of the cellular elements related to cell-mediated fnosecae involved in the inflammatory response to chromoblastomycosis in skin lesions.

Studies in athymic mice infected with F. Immunization of mice with living F. These cells were purified from mice and, in vitroproliferated after restimulation with specific antigen designated as chromoAg, which corresponds to the cell-free culture supernatant obtained pedrlsoi F. T cells from these individuals fail to proliferate in vitro after induction with chromoAg. The host receptors involved in the immune response to chromoblastomycosis still remain to be characterized. In vitro studies demonstrated that, in the presence of chromoblastomycosis agents, the expression of MHC-II and CD8 molecules in pwdrosoi is down modulated Hayakawa et al.

In addition, phagocytosis of F. Pesrosoi binding of fungal antigens to host receptors, however, remains to be demonstrated. Melanin, a major F. The knowledge on the structure of cell wall components of F. Finally, mannose-bearing structures, which were previously described as surface structures of F.

Chromoblastomycosis treatment is difficult and most therapeutic attempts provide only a modest success rate Bonifaz et pedrpsoi. Moreover, the response to oral antimycotic drugs is limited Minotto et al. Several treatment regimes have been used to treat chromoblastomycosis but long-term efficacy is still too low to allow specialists to elect a drug of choice McGinnis et al.

For some cases, the best therapeutic strategy in cases of chromoblastomycosis seems to be a combination of two drugs chosen according to the results of prior antifungal susceptibility testing Poirriez et al. The widespread use of antifungal associated with long-term treatment might lead to fungal resistance producing relapses during therapy Espinel-Ingroff et al.

Tests in vitro revealed that caspofungin is active against F. On the other hand, fluconazole and ketoconazole have no practical activity De Bedout, ; Andrade et al. Other alternative therapies include physical methods such as conventional surgery, laser surgery, thermotherapy and cryotherapy Bonifaz et al. Among them, surgical treatment appears to be the most effective choice to manage chromoblastomycosis.


Surgery, electrodessication and cryosurgery are more effective in early stages Lupi et al. Local heat can reduce substantially the extension of the lesions and the need for extensive surgeries.

;edrosoi A successful therapy of F. Disabled or deformed limbs may require amputation Elgart, Fonsecaea pedrosoi is one of the most frequent causative agents of chromoblastomycosis Rippon et al. Although considered a worldwide-distributed fungus, F. Its natural niche is the same described for other dematiaceous species, which comprise soil, rotten wood and decomposing fonsceae material Rippon et al. The colonies mature usually in 14 days and are olivaceous to brown-black in color Fig.

Fonsecaea produces septate, dark brown hyphae and erect conidiophores that highly branch at apices Fig. Cultures of Fonsecaea pedrosoi on Sabouraud dextrose agar. A velvety, dark fungal colony of F. Heaped and granular colonies with a black surface are shown in b. An aqueous solution of melanin, the dark pigment of F. Morphologies of Fonsecaf pedrosoi observed by light a, b and scanning electron microscopy c.

Mycelial cells, including conidial formation arrowsare shown in a. Inset in a shows isolated conidia. Sclerotic cells, the parasitic forms of F. Inset in b shows disarticulated sclerotic cells.

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Scanning electron microscopic images of each fungal form and the potential forms of differentiation are shown in c. Fonsecaea pedrosoi is a valuable model in cell biology.

As discussed above, its life cycle comprises different morphological states that include reproduction structures conidia and fungal forms usually found in the saprophytic mycelia and parasitic stage sclerotic bodies Fig. The mechanisms involved in the morphological transitions of F.

Fonsecaea pedrosoi

Many fonsecaae are involved in fungal morphogenesis, including nutritional elements, temperature and aerobic conditions Szaniszlo et al. However, the difficulty in inducing sclerotic cells in vitro has resulted in a lack of physiological studies with the tissue forms of F. Acidic ranges of pH are considered to be key inducers of the formation of sclerotic cells Cooper et al.

This study was further validated by Silva et al. It has also been described that F. Although the conditions that induce morphological transitions and consequent sclerotic cell formation during infection are unknown, a potential physiological inducer of the F.

Electron microscopy techniques confirmed that PAF induced the formation of typical sclerotic cells, as previously described with propranolol Alviano et al. In addition, several biochemical parameters were evaluated in PAF and propranolol-induced ledrosoi. They both presented similar profiles of fatty acid constituents, polysaccharide composition and surface carbohydrate expression Alviano et al. The addition of PAF or propranolol to mycelial cultures similarly stimulated ectophosphatase activity, supporting a correlation between morphogenesis and surface expression of phosphatases Kneipp et al.

Sclerotic cells are extremely resistant to pesrosoi by immunological action Esterre et al. In this context, inhibition of the differentiation of F. Therefore, the understanding of this process and, consequently, how this morphological transition can be inhibited may allow the design of alternative and efficient therapies against chromoblastomycosis. Therefore, besides the host cells regularly present in infected tissues, effector cells that are recruited to the sites of infection are key elements in the immune response to subcutaneous mycoses Hayakawa et al.