Introduction
Background
Chromoblastomycosis is a chronic fungal infection of the skin and the subcutaneous tissue caused by traumatic inoculation of a specific group of dematiaceous fungi (usually Fonsecaea pedrosoi, Phialophora verrucosa, Cladosporium carrionii, or Fonsecaea compacta) through the skin.1
Several cases of infection by Exophiala species have appeared in the literature.2 Chromoblastomycosis is classified among the subcutaneous mycoses and is ubiquitous; however, the prevalence is higher in rural populations in countries with a tropical or subtropical climate, such as Madagascar in Africa and Brazil in South America.
Nomenclature
Since its identification in the early 1910s, the name of the disease has been frequently misused to encompass other infections caused by dematiaceous fungi. More recently, the advent of immunosuppressive therapies and diseases brought more confusion because of the identification of new agents and clinical settings. With the introduction of the concept of phaeohyphomycosis by McGinnis in 1983,3 differentiation among these diseases became more obvious. The features of chromoblastomycosis are distinctive enough to consider chromoblastomycosis an independent clinical entity. The infection should not be confused with mycoses, such as mycetoma or phaeohyphomycosis, caused by other dematiaceous fungi.
Nowadays, the term chromoblastomycosis is restricted to the cases in which sclerotic cells are present in tissue. Sclerotic cells, also known as Medlar bodies, are globe-shaped, cigar-colored, thick-walled structures that are 4-12 µm in diameter (see Media File 1).
Sclerotic cells on a potassium hydroxide preparation.
Medlar first described them in 1915.4 These structures multiply by septation, and they induce a purulent and granulomatous inflammatory reaction in tissue (see Histologic Findings).
In 1992,5 the International Society for Human and Animal Mycology (ISHAM) recommended that the best name to define the disease was chromoblastomycosis, which Terra et al coined in 1922.6
History
Contrary to what appears in some textbooks, chromoblastomycosis was first described by Max Rudolph in 1914 and not by Lane7 or Medlar4 in 1915. In 1987, Castro and Castro8 reported that Max Rudolph, a German physician living in Brazil, published a preliminary communication where the first 6 cases of the disease were described. Rudolph was also able to isolate a dark-colored fungus from 4 of 6 patients; this fungus grew in culture as a dark grey-to-black–colored furlike colony. Rudolph believed this fungus to be a type of blastomycete, and he successfully inoculated the disease in 4 white rats and 2 monkeys. Surprisingly, he did not describe the histologic aspects of the disease or the pathognomonic sclerotic cells, which both Lane and Medlar described 1 year later.
In 1928, Hoffman9 mentioned that in Cuba in 1908 Guiteras had observed 10 cases of a disease known as chapa in which the clinical aspects resembled those of chromoblastomycosis. Unfortunately, those cases were not published. In 1920, 2 Brazilian physicians, Pedroso and Gomes,10 published 4 cases that had been under observation for many years, the first one since 1911. According to them, all 4 cases were caused by P verrucosa. Two years later, in 1922, Brumpt11 concluded that the agents isolated by Pedroso and Gomes could not be classified as Phialophora species, and he coined the denomination Hormodendrum pedrosoi, later renamed F pedrosoi by Negroni12 in 1936. By 1930, new cases had been described outside the American continent in France, Sumatra, and Poland.13
Four different genera are now widely accepted to cause chromoblastomycosis: F pedrosoi, P verrucosa, C carrionii, and F compacta.14 Rare cases of chromoblastomycosis caused by Rhinocladiella aquaspersa and Exophiala species have also been reported, allowing the inclusion of these species among those that cause the disease.15,16,17,18,19
Pathophysiology
The infection usually results from a traumatic cutaneous injury that is often not remembered or realized by the patient. The agents often gain entry into the human body by contact with wood splinters or thorns.
The fungi most commonly reported as causing chromoblastomycosis are F pedrosoi, C carrionii, and P verrucosa. A small number of cases due to F compacta, R aquaspersa, and different species of Exophiala have also been reported. In 2007, Chaetomium funicola was identified as a cause of chromoblastomycosis in Panama.20
Several authors have demonstrated that a number of different dematiaceous fungi can be isolated from nature. In 1937, Conant21 demonstrated that a fungus called Cadophora americana, which was isolated from timber, was actually the same organism as P verrucosa. Later isolations were obtained in several countries from materials, such as plants, palm trees, grass, and soil.18 C carrionii has been isolated from cactaceae, both from the thorns and from the medullae, in Venezuela.22 C carrionii is the most common agent of chromoblastomycosis in that country, and trauma due to plants is believed to inoculate the skin with the fungus. The fungal cells in human tissue present with the same features as those observed in the inner portions of the plants.
The lesions develop slowly at the site of implantation, producing a warty nodule, which tends to be limited to the skin and the subcutaneous tissue. Over the years, the nodule grows centripetally. In many instances, the central parts of the lesion heal, leaving ivory-colored scars. The disease tends to spread to neighboring healthy skin, forming plaques, which, at times, can involve a whole limb. When nodular lesions predominate over the plaques, the disease assumes a typical cauliflower aspect. Both lymphatic dissemination and cutaneous dissemination have been described.
Frequency
International
The disease has been described worldwide, but the incidence is greater in tropical and subtropical regions located between 30° N and 30° S.23
An estimated 20% of cases are found in temperate climates, such as in Japan,24 Canada,25 Finland,26,27 and Romania and the Czech Republic.13 Chromoblastomycosis most commonly affects male agricultural workers in rural regions of North America, Central America, and South America, but chromoblastomycosis does occur worldwide, including Europe, England, India, South Africa, and Australia. The highest incidence of chromoblastomycosis in the world is in the African country of Madagascar, and a large number of cases have been reported in Japan. A survey in the Brazilian Amazon disclosed an extremely high incidence of chromoblastomycosis (1.6 cases per 10,000 population) in a village called Monte Negro, in the state of Rondonia.
Countries with the highest number of cases are Madagascar and Brazil. Several different African and Latin American countries, such as Gabon, Colombia, Venezuela, Cuba, the Dominican Republic, and Mexico, also have high prevalence rates.
F pedrosoi infection is most commonly observed in humid climates, whereas C carrionii infection is normally found in dry areas.
Farming is the most common occupation in patients with chromoblastomycosis.28
Fonsecaea monophora is the predominant etiologic agent of chromoblastomycosis in southern China.29
Mortality/Morbidity
- Mortality due to chromoblastomycosis is a rare event.
- Morbidity relates directly to the severity of the disease. Initially, in the papule or nodule phase, the disease is asymptomatic. When the nodules coalesce, forming large plaques and sometimes involving the whole limb, complications may appear.
- Common complications include ulceration, lymphedema, and secondary infection.
Race
No racial predilection is reported.
Sex
Most series reports indicate a clear male predominance, although a small number of reports describe similar male-to-female ratios.
- Approximately 70% of cases are seen in men. The explanation for this male 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, rather than women who are supposedly more dedicated to house jobs.
- The possible inhibitory effect of female hormones on the growth of fungi may partially explain the relatively low number of cases in females.
Age
Patients with the disease are most commonly aged 30-50 years.
- The period between inoculation and disease development is believed to last years, explaining the scarcity of children with chromoblastomycosis.
- The disease is rarely found in children exposed to the same environmental conditions as adults.
Clinical
History
Patients usually do not report discomfort, and they tend to not seek medical care until secondary infection or elephantiasis ensues.
Physical
The disease appears at the site of a previous often unnoticed or unremembered trauma to the skin. After several years, a small, raised, erythematous, asymptomatic papule develops. As the chromoblastomycosis lesion develops over years, it assumes a scaly and infiltrated aspect, generally leading to either of the 2 most common clinical variants: nodular or plaque. In both types, the surface is verrucous, and lesions spread laterally to contiguous healthy tissue.
Chromoblastomycosis, tumoral form. Chronic disease led to elephantiasis and involvement of the entire lower limb.
Plaque lesion on the foot. The verrucous aspect of the lesion differentiates it from other infectious dermatoses that may present as a verrucous lesion, namely, cutaneous leishmaniasis, sporotrichosis, cutaneous tuberculosis, and cutaneous mycobacteriosis.
In general, the disease remains localized to the area of the initial infection or neighboring skin, but lymphatic and hematogenous dissemination may occur, producing metastatic lesions away from the primary site. The nodular type of lesion normally develops into verrucous, pedunculated, cauliflowerlike florets, while the plaque type spreads peripherally, with an active, raised border, leaving a central healed area with atrophic and yellowish scar tissue.
On the surface of both types of clinical variants, numerous black dots may be observed where the causative organisms are preferentially found. Hemopurulent material covering small ulcerations is commonly observed.
Cutaneous localized annular chromoblastomycosis has been described as well-circumscribed, slow-growing, annular, papulosquamous or papulosquamous-verrucous patches or plaques with no regression despite the use of topical antifungals.30
Secondary infection with bacteria is common, giving the lesion a characteristic ill odor. Secondary infection is believed to be important in the genesis of lymph stasis and consequently of elephantiasis. In old cases, lesions in different stages of development can be found. Extracutaneous spread may occur rarely, due to hematogenic and lymphatic dissemination. Contiguous spread to the underlying bone may produce an osteolytic lesion.31
The sites most commonly affected are the lower extremities, especially the feet. The hands, the arms, and the buttocks are also frequently involved, and sporadic reports mention lesions on the ears, the face, and the breasts.
Causes
The isolation of the causative fungi from nature on several different occasions has added to the demonstration that fungi gain entry into the host's body through traumatic inoculation1 ; this finding also confirmed that populations at risk are rural workers who walk barefoot in endemic regions where the causative agents are found.
- A Brazilian study has suggested a link between the occurrence of lesions on the buttocks and the habit of sitting on babaçu (Orbignya phalerata) shells. The authors have failed to isolate the causative fungus from the shells.32 In 2004, Salgado et al33 were able to isolate the same F pedrosoi from a thorny bush (Mimosa pudica) and from a chromoblastomycosis patient. The lesion had developed after an accident at the site where those bushes grew.
- On the other hand, in 1994, Zeppenfeldt et al22 demonstrated that certain cactaceae from the Falcon state in Venezuela had fungi not only on their surfaces and thorns but also in the medulla. Not coincidentally, the fungus was identified as C carrionii, which is the most commonly found organism in chromoblastomycosis cases in that country. The histologic characteristics of the fungus in plant tissue resembled that found in humans. Experimental inoculation of C carrionii in goats, performed n Venezuela, demonstrated that although chromoblastomycosis affecting that genus of mammals has never been reported, C carrionii caused cellular reactions in goats identical to those seen in humans at the first stages of infection.34
- In 1989, Tsuneto et al35 demonstrated a higher frequency of HLA-A29 in patients with chromoblastomycosis; this finding suggests that genetics might have an influence in the acquisition of the disease.
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Further Reading
Keywords
chromomycosis, fungal infection of the skin, dematiaceous fungi, Fonsecaea pedrosoi, F pedrosoi, Cladosporium carrionii, C carrionii, Phialophora verrucosa, P verrucosa, Fonsecaea compacta, Rhinocladiella aquaspersa, R aquaspersa, Exophiala species, sclerotic cells
