Chromoblastomycosis
Introduction
Chromoblastomycosis (formerly chromomycosis) is a chronic, progressive, subcutaneous mycosis caused by pheoid or dematiaceous fungi. The latter is a group of pigmented black fungi, which belong mainly to the Fonsecaea, Phialophora, and Cladophialophora spp. All of the causative agents generate the same parasitic forms, known as fumagoid cells or Medlar bodies. These are dark, oval thick walled cells with septation or binary fission.1., 2., 3., 4., 5. Chromoblastomycosis is characterized by warty nodular lesions, usually involving the legs.1 Most patients have a history of trauma caused by wood or vegetation, and more than 80% are agricultural workers, who often go barefoot (Fig. 1, Fig. 2, Fig. 3, Fig. 4, Fig. 5, Fig. 6, Fig. 7).1
Section snippets
History
Chromoblastomycosis was first noted in Brazil in 1911 by de Moraes Pedroso, but it was not reported until 1920 by Pedroso and Gomes. In 1914, Max Rudolph emphasized the clinicopathologic features, and Medlar and Lane reported the first North American case in Boston in 1915. At that time, the isolated fungus was called Phialophora verrucosa. In 1922, Pedroso’s original culture was restudied and different types of reproduction were noted, including Hormodendrum, Phialophora, and Acrotheca. As a
Epidemiology
Chromoblastomycosis has a worldwide distribution and is frequently seen in tropical and subtropical climates. Most cases are from Madagascar (the most important focus in the world), but many cases have been reported from Gabon, Mexico, Brazil, Costa Rica, Puerto Rico, Venezuela, Cuba, Dominican Republic, India, and Australia. Chromoblastomycosis has been diagnosed in several countries in Europe.5 Between 1955 and 1980, 290 cases were reported in Japan, and 249 of these were caused by F pedrosoi.
Etiology and pathogenesis
Several species of Hyphomycetes of the Dematiaceae family have been isolated. The most frequent etiologic agents are: F pedrosoi, F compacta, Phialophora verrucosa, Cladophialophora carrionii, and Rhinocladiella aquaspersa (Table 1). These agents are slow-growing fungi with low virulence and a high tolerance to heat (40°-42ºC).1
The pathogenesis of chromoblastomycosis is not fully understood. A genetic susceptibility is suggested by the development of several cases in a family, although this has
Etiologic agents
The agents of chromoblastomycosis are common soil saprophytes of decaying wood and plants. They penetrate through a skin abrasion and spread by contiguity. These fungi have also been isolated in wood from sauna baths in Finland, which corroborates their resistance to high temperatures. F pedrosoi is the most important agent in tropical zones of Latin America, with a high frequency in rural populations in Cuba, Puerto Rico, and the Dominican Republic. It is also the most common etiologic agent
Clinical features
The incubation period is unknown. A history of injury or traumatic inoculation is not always present.2 The lesions are more frequent on the legs (85%).1 The disease can also involve other exposed areas, such as hands, arms, trunk, buttocks, neck, forearms, and face. Less than 20% of patients develop disseminated lesions affecting both the arms and legs. Initially, the lesion is a small, nonpruriginous, erythematous papule that slowly spreads to the surrounding skin. New lesions develop over
Diagnosis
The characteristic finding on direct examination with potassium hydroxide (KOH) is the presence of sclerotic or fumagoid cells (Medlar bodies [Figure 5]). These are double-walled brown structures with a diameter of 4 to 10 µm that resemble copper pennies. Sometimes, thick and dark hyphae are identified. Cultures can be performed on Sabouraud agar or Sabouraud with antibiotics at 25° to 28ºC. The organism grows slowly (25-30 days).
The biopsy specimen shows pseudoepitheliomatous hyperplasia with
Differential diagnosis
The most important differential diagnoses are verrucous tuberculosis, fixed sporotrichosis, lacaziosis, leishmaniasis, blastomycosis, paracoccidioidomycosis, verrucae, and squamous cell carcinoma.1., 5.
Treatment
Chromoblastomycosis is extremely difficult to treat and is often refractory to various therapeutic approaches. Reliable therapies include curettage, electrodesiccation, and cryosurgery. Drug therapy for at least 6 months may result in a favorable clinical response, but relapses during or after therapy are common.
In early or small lesions, a wide and deep excision is the treatment of choice. A common approach involves monthly cryosurgery sessions combined with oral itraconazole (300-400 mg/d)
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