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School of Biological Sciences
The University of Adelaide

Dr David Ellis



A mycotic infection of the cutaneous and subcutaneous tissues characterised by the development in tissue of dematiaceous (brown-pigmented), planate-dividing, rounded sclerotic bodies. Infections are caused by the traumatic implantation of fungal elements into the skin and are chronic, slowly progressive and localised. Tissue proliferation usually occurs around the area of inoculation producing crusted, verrucose, wart-like lesions. World-wide distribution but more common in bare footed populations living in tropical regions. Aetiological agents include various dematiaceous hyphomycetes associated with decaying vegetation or soil, especially Phialophora verrucosa, Fonsecaea pedrosoi, F. compacta and Cladophialophora carrionii.

Clinical manifestations:

Lesions of chromoblastomycosis are most often found on exposed parts of the body and usually start a small scaly papules or nodules which are painless but may be itchy. Satellite lesions may gradually arise and as the disease develops rash-like areas enlarge and become raised irregular plaques that are often scaly or verrucose. In long standing infections, lesions may become tumorous and even cauliflower-like in appearance. Other prominent features include epithelial hyperplasia, fibrosis and microabscess formation in the epidermis. Chromoblastomycosis must be distinguished from other cutaneous fungal infections such as blastomycosis, lobomycosis, paracoccidioidomycosis and sporotrichosis. It may also mimic protothecosis, leishmaniasis, verrucose tuberculosis, certain leprous lesions and syphilis. Mycological and histopathological investigations are essential to confirm the diagnosis.

white verrucoid cutaneous lesion on the handwhite verrucoid cutaneous lesion on the hand
Chronic verrucous chromoblastomycosis of the hand due to Cladophialophora carrionii.

Note: tissue hyperplasia forming a white verrucoid cutaneous lesion. In Australia, chromoblastomycosis due to C. carrionii occurs mostly on the hands and arms of timber and cattle workers in humid tropical forests.

Laboratory diagnosis:

1. Clinical Material: Skin scrapings and/or biopsy.

2. Direct Microscopy: (a) Skin scrapings should be examined using 10% KOH and Parker ink or calcofluor white mounts; (b) Tissue sections should be stained using H&E, PAS digest, and Grocott's methenamine silver (GMS).

Interpretation: The presence in tissue of brown pigmented, planate-dividing, rounded sclerotic bodies from a patient with supporting clinical symptoms should be considered significant. Remember direct microscopy or histopathology does not offer a specific identification of the causative agent. Note: direct microscopy of tissue is necessary to differentiate between chromoblastomycosis and phaeohyphomycosis where the tissue morphology of the causative organism is mycelial.

Skin scrapings mounted in 10% KOH
Skin scrapings from a patient with chromoblastomycosis mounted in 10% KOH and Parker ink solution showing characteristic brown pigmented, planate-dividing, rounded sclerotic bodies.

H&E stained section
H&E stained section showing characteristic dark brown sclerotic cells which divide by binary fission and not by budding. Note all agents of chromoblastomycosis form these sclerotic bodies in tissue.

3. Culture: Clinical specimens should be inoculated onto primary isolation media, like Sabouraud's dextrose agar.

Cultures of the aetiologic agents of chromoblastomycosis are typically olivaceous-black with a suede-like surface.

Interpretation: The dematiaceous hyphomycetes involved are well recognised as environmental fungi, therefore a positive culture from a non-sterile specimen, such as sputum or skin, needs to be supported by clinical history and direct microscopic evidence in order to be considered significant. Culture identification is the only reliable means of distinguishing these fungi.

4. Serology: There are currently no commercially available serological procedures for the diagnosis of chromoblastomycosis.

5. Identification: Culture characteristics and microscopic morphology are important, especially conidial morphology, the arrangement of conidia on the conidiogenous cell and the morphology of the conidiogenous cell. Cellotape flag and/or slide culture preparations are recommended.

Causative agents:

Cladophialophora carrionii, Fonsecaea pedrosoi, Phialophora verrucosa


The treatment of chromoblastomycosis has been exceedingly difficult. Successful surgical excision requires the removal of a margin of uninfected tissue to prevent local dissemination. Flucytosine with or without thiabendazole has been extensively used in the past. However both itraconazole [400 mg/day] and terbinafine [500 mg/ day] for 6 to 12 months have been used successfully for the treatment of chromoblastomycosis.

Further reading:

Ajello L and R.J. Hay. 1997. Medical Mycology Vol 4 Topley & Wilson's Microbiology and Infectious Infections. 9th Edition, Arnold London.

Esterre P, Inzan CK, Ramarcel ER, Andriantsimahavandy A, Ratsioharana M, Pecarrere JL, Roig R, Treatment of chromomycosis with terbinafine: preliminary results of an open pilot study. Br J Dermatol (1996) 134 (Suppl. 46):33-36.

Kwon-Chung KJ and JE Bennett 1992. Medical Mycology Lea & Febiger.

Richardson MD and DW Warnock. 1993. Fungal Infection: Diagnosis and Management. Blackwell Scientific Publications, London.

Rippon JW. 1988. Medical Mycology WB Saunders Co.