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Treating Rare Fungal Infections: Chromoblastomycosis

Treating Rare Fungal Infections: Chromoblastomycosis

This feature series was taken from the 4th annual postgraduate course and workshop in medical 

mycology-dermatomycology from July 27-30, 1979 in Newport Beach, CA.

Dr. Graham was the former head of dermatopathology at the Armed Forces Institute of Pathology and the former chair of dermatology at UC Irvine in Irvine, CA. He has made available his personal library of kodachromes, slides and lectures collected throughout his career with a generous donation to the Wake Forest University Baptist Medical Center library. Dr. Graham’s lectures and personal images in dermatomycology will be highlighted in this series to refresh the practicing clinician on deep cutaneous mycotic disease.


Chromoblastomycosis, or chromomycosis, is a subcutaneous, dematiaceous fungal infection, resulting from skin inoculation by pigmented fungi including Fonsecaea pedrosoi, Phialophora verrucosa, Cladophialophora carrionii, Fonsecaea compacta and Wangiella dermatitidis.1 F. pedrosoi and C. carrionii are the most common causes of chromoblastomycosis.2   

The infection was first identified in the early 1910s and the first several cases were described in Brazil in the 1920s.3 Chromoblastomycosis was once considered a disease of rural workers but is now being discovered in people working other sectors.4 While chromoblastomycosis is not characterized as a fatal disease, it is a slow-to-develop, chronic infection associated with poor treatment outcomes and persistent relapse rates.

Epidemiology and Pathogenesis

Most pigmented fungi are found within environments that contain wood, plant debris or soil. These mycoses are usually isolated in subtropical and tropical climates, particularly Central and South America, Africa, Japan and Australia.3 Fonsecaea pedrosi is the most common etiologic agent and is found in tropical rainforests with high amounts of rainfall, including the Amazon and the temparate regions of Central and South America.5 Cladophialophora carrionii is the main infectious agent in dry countries and desert regions, particularly Australia, South Africa and Cuba.5 These saprophytic fungi implant into the skin following traumatic injury, particularly in areas not protected by clothing or shoes.4 Because infection occurs from traumatic implantation of the skin, it is frequently seen in rural agricultural workers and farmhands, especially those who are barefoot.5 Chromoblastomycosis is commonly seen in males and occurs after adolescence, though it can infect individuals of any age.5 

fungal foot

Figure 1. Chromoblastomycosis presenting on the toes, foot and ankle. Source: Graham Library of Digital Images, Wake Forest University Department of Dermatology © 2009 Wake Forest University Dermatology

Clinical Presentation 

The inital site of infection is usually on the arms, upper trunk, legs or feet because those areas are least likely to be covered by clothing or protective gear. Unusual sites of infection in the genitalia and nose have been reported.3,5 The clinical presentation of the lesions varies and includes 5 distinct appearances: nodular lesions with raised surfaces that are covered by cauliflower-like scabs; extensive tumoral lesions; extensive, irregular, verrucose, hyperkeratotic lesions; reddish, flat, scaly plaques; and cicatricial atropic skin lesions with sparing at the center.2-4 Of these, nodular and verrucose hyperkeratotic lesions are most common, especially in the initial stages of infection. 

Early lesions form at the site of innoculation and spread slowly over several weeks to months. Skin lesions may be mildly pruritic or even asymptomatic, unless other complications like ulceration, secondary bacterial infection or lymphadenopathy occur. The infection is most often localized and limited to the subcutaneous tissue. Satellite lesions can appear due to auto-inoculation through scratching and from lymphatic distribution.2,5 After several years, the lesions can develop into tumoral-like, cauliflower-shaped masses, or they can heal leaving sclerotic plaques or keloids.5 Although rare, these lesions can undergo malignant transformation into squamous cell carcinoma.5 

culture stain

 Figure 2. Chromoblastomycosis. Culture stained with 10% KOH revealing the Medlar bodies, muriform bodies or sclerotic cells with round, brown, thick-walled and multi-septate cells. Source: Graham Library of Digital Images, Wake Forest University Department of Dermatology © 2009 Wake Forest University Dermatology


Histopathological examination reveals a granulomatous process with marked epithelial hyperplasia, lymphohistiocytic infiltrate with neutrophils and the presence of muriform cells.5 Inflammatory infiltrate with multinucleated cells, fibrosis, acanthosis, papillomatosis, hyperkeratosis and pseudoepitheliomatous hyperplasia may be seen histologically.2 The organism may be visible in giant cells or in neutrophil abscesses and appears singly or in small groups of brown pigment cells, often with a single or double septum and thick cell wall.2,5-7 

fungal slide

Figure 3. Chromoblastomycosis. Histological sample stained with hematoxylin and eosin showing the brown-pigmented Medlar bodies.  Source: Graham Library of Digital Images, Wake Forest University Department of Dermatology © 2009 Wake Forest University Dermatology

Differential Diagnosis

Because of the diverse presentation of lesions of chromoblastomycosis, the differential diagnosis is quite large. The differential diagnosis of chromoblastomycosis includes leishmaniasis, tuberculosis, sporotrichosis, protothecosis, lupus erythematosus, leprosy, cutaneous granuloma, cutaneous sarcoidosis and squamous cell carcinoma, all of which may produce verrucous-like lesions.2,8 Microscopic examination of the lesions using KOH stain is considered sufficient to confirm chromoblastomycosis and disregard the other possible causes of the lesions, but culture identification is the gold standard for diagnosis.2,5 

fungal slide2

 Figure 4. Chromoblastomycosis. Inflammatory infiltrate and multi-nucleated cells surrounding the infected Medlar bodies. Medlar bodies or sclerotic cells are found in the tissue of patients and are characteristically globe-shaped, cigar-colored and have thick walls (4-12 µm in diameter). Source: Graham Library of Digital Images, Wake Forest University Department of Dermatology © 2009 Wake Forest University Dermatology

Diagnostic Tests

To diagnose chromoblastomycosis, lesion scrapings must be examined under a microscope in KOH stain (10% potassium hydroxide).5 Medlar bodies, muriform bodies or sclerotic cells will be visible with the potassium hydroxide stain as round, brown, thick-walled and multi-septate cells.3-5,7 Lesions that are more likely to yield a positive result have black dots visible on the surface of lesion.2,5 These black dots represent transepidermal elimination of the fungal agents and scrapings should be taken around these black dots if possible.2,5 Skin scrapings are also stained with hematoxylin and eosin to reveal the Medlar bodies.5

A culture of the lesion is necessary to identify the particular species responsible for the infection, but the slow growth of these fungi and poor morphological differentation among species makes it difficult to identify the species. Scrapings or biopsy fragments should be cultured using Sabouraud dextrose agar.2 The subsequent colonies should appear velvety within 10 days. Identification is made by microscopically visualizing the asexual reproductive structures.2 PCR assays are also available for the identification of Fonsecaea species and C. carrionii

fungal slide3

 Figure 5. Chromoblastomycosis. Pseudoepitheliomatous hyperplasia and fibrosis. Source: Graham Library of Digital Images, Wake Forest University Department of Dermatology © 2009 Wake Forest University Dermatology


Chromoblastomycosis has low cure rates and high relapse rates. Treatment options depend on several factors: the etiological agent; the size and extent of the lesions; the clinical topography; and the presence of complications. The most common agent, F. pedrosi, is also the least sensitive to antifungal therapy. 

The main treatments for chromoblastomycosis are itraconazole 200 mg daily, terbinafine 250 mg daily, flucytosine 50-150 mg/kg per day in 4 doses, fluconazole 200-600 mg/day, ketoconazole 200-400 mg/day, or, in extreme cases, intravenous amphotericin B up to 1 mg/kg daily.2,3,5-9 Itraconazole, amphotericin B and thiabendazole are often administered in combination with flucytosine. Surgery can be undertaken if the lesions are small, but the risk of spreading the infection is a major concern.

In addition to the above treatments, local heat applied to small lesions has a modest effect for reducing their size.7,10 Cryotherapy once a month has promising results when used with thiabendazole.7,11,12 Local heat and cryotherapy should only be utilized for smaller lesions, while combination therapy is recommended for moderate-to-severe forms of chromoblastomycosis.7,10-12 The best results have been seen with itraconazole and terbinafine at high doses for 6-12 months.9

Successful treatment is contingent on the causal agent and the severity of disease. Small lesions caught at an early stage respond best. Treatment should be continued until the lesions resolve, which usually takes several months of therapy. Relapse is unfortunately very common with chromoblastomycosis.9-12

Key Points

• Chromoblastomycosis is a chronic, subcutaneous, mycotic infection caused by pigmented saprophytic fungi found primarily in soil, wood and plant debris. 

• The most common etiologic agents are Fonsecaea pedrosoi and Cladophialophora carrionii.

• Chromoblastomycosis is seen in tropic and subtropical climates, particularly Central and South America, Africa, Australia and Japan. 

• Infection is due to traumatic inoculation of the organism into the skin and is commonly seen on hands, feet, legs, arms and other areas that are not protected by clothing. 

• The slow-growing infection has various presentations at the site of inoculation, but the most common lesions are wart-like papules or verrucose plaques. 

• Direct microscopic examination of lesion scrapings using KOH is required to identify chromoblastomycosis.

• Histopathological exam reveals an inflammatory process with neutrophils, multinucleated cells, fibrosis and the presence of round, brown, thick-walled, multi-septate muriform cells inside the giant cells or neutrophils. 

• Treatment options include itraconazole, fluconazole, flucytosine, terbinafine, amphoterin B and ketoconazole for several months until clinical symptoms resolve. 

• Relapse is common and cure rates are very low for chromoblastomycosis. 


Ms. Culp is with Center for Dermatology Research, and the department of dermatology at Wake Forest School of Medicine in Winston-Salem, NC. 

Mr. Al-Dabagh is a 4th year medical student at Case Western Reserve University School of Medicine in Cleveland, OH. 

Dr. Feldman is with the Center for Dermatology Research and the Departments of Dermatology, Pathology and Public Health Sciences at Wake Forest University School of Medicine.


Disclosures: The Center for Dermatology Research is supported by an unrestricted educational grant from Galderma Laboratories, L.P.  Dr. Feldman is a consultant and speaker for Galderma, Stiefel/GlaxoSmithKline, Abbott Labs, Warner Chilcott, Janssen, Amgen, Photomedex, Genentech, BiogenIdec, and Bristol Myers Squibb. Dr. Feldman has received grants from Galderma, Astellas, Abbott Labs, Warner Chilcott, Janssen, Amgen, Photomedex, Genentech, BiogenIdec, Coria/Valeant, Pharmaderm, Ortho Pharmaceuticals, Aventis Pharmaceuticals, Roche Dermatology, 3M, Bristol Myers Squibb, Stiefel/GlaxoSmithKline, Novartis, Medicis, Leo, HanAll Pharmaceuticals, Celgene, Basilea, and Anacor and has received stock options from Photomedex. He is owner of and a founder of Causa Research. Ms. Culp and Mr. Al-Dabagh have no conflicts to disclose.



1. Esterre P. Chromoblastomycosis. In: WG Merz, RJ Hay, ed. Topley and Wilson’s Microbiology and Microbial Infections: Medical Mycology. London: Hodder Arnold; 2004: 356.

2. López MR, Tovar M. Chromoblastomycosis. Clin Exp Dermatol. 2007;25(2):188-194.

3. Correia RT, Valente NY, Criado PR, Martins JE. Chromoblastomycosis: Study of 27 cases and review of medical literature. An Bras Dermatol. 2010;85(4):448-54. 

4. Goette DK, Robertson D. Transepithelial elimination in chromomycosis. Arch Dermatol. 1984;120(3):400-401.

5. Ameen M. Chromoblastomycosis: Clinical presentation and management. Clin Exper Dermatol. 2009;34(8):849-854. 

6. Lupi O, Tyring, SK, McGinnis, MR. Tropical dermatology: fungal tropical diseases. J Am Acad Dermatol. 2005;53(6):931-951. 

7. Bonifaz A, Saúl A, Paredes-Solis V, Araiza J, Fierro-Arias L. Treatment of chromoblastomycosis with terbinafine: Experience with four cases. J Dermatol Treat. 2004;16(1):47-51.

8. Restrepo A. Treatment of tropical mycoses. J Am Acad Dermatol. 1994;31:S91-S102. 

9. Garnica M, Nucci M, Queiroz-Telles F. Difficult mycosis of the skin: Advances in epidemiology and management of eumycetoma, phaeohyphomycosis and chromoblastomycosis. Curr Opin Infect Dis. 2009;22(6):560-565. 

10. Hirume H, Kawada A, Yoshida M, Kouya M. Hyperthermic treatment of chromomycosis with disposable chemical pocket warmers. Mycopathologia. 1993;122(2):107-114. 

11. Hiruma M, Ohsishi Y, Ohata H, et al. Chromomycosis of the breast. Int J Dermatol.1992;31(3):184-185. 

12. Bonifaz A, Martinez-Soto E, Carassco-Gerard E, Peniche J. Treatment of chromoblastomycosis with itraconazole, cryosurgery and a combination of both. Int J Dermatol. 2008;36(7):542-549. 

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