Conditions · Infectious and tropical diseases
Chromoblastomycosis !
A slow, chronic fungal skin infection of rural workers, entering by a thorn or splinter, that forms warty plaques, usually on the leg or foot.
Updated 2026-11-01
Structures involved
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Why it happens
- Granulomatous inflammation: caseating vs non-caseating, the causes to know
- Hyperplasia: physiologic and pathologic
- Skin: epidermis layers, dermis, hypodermis
What it is
Chronic infection of the skin and subcutaneous tissue by dark-pigmented (dematiaceous) fungi that live in soil and plants. After minor trauma, a small papule grows over years into warty nodules and plaques, mostly on the lower limb. It is one of the implantation mycoses and is considered a neglected tropical disease.
Who gets it
Occurs in tropical and subtropical areas, with the highest numbers in Brazil, Madagascar, Mexico, Venezuela and parts of Asia; Colombia reports cases mainly in rural agricultural areas. It typically affects adult men aged 30–60 who work barefoot or with little protection in farms or forests. Fonsecaea species predominate in humid regions and Cladophialophora carrionii in dry, semiarid zones such as Falcón state in Venezuela.
Causes
- Dematiaceous fungi, mainly Fonsecaea pedrosoi and related species
- Cladophialophora carrionii in arid areas; Phialophora verrucosa and Rhinocladiella aquaspersa less often
- Traumatic implantation by thorns, splinters, wood or plant material
- Not transmitted from person to person
Risk factors
- Agricultural or forestry work, wood cutting and plant handling
- Walking barefoot and not wearing gloves
- Male sex and adult age
- Rural residence in tropical or semiarid regions; immunosuppression may worsen disease
Pathophysiology
The fungus enters the dermis through a wound and converts into thick-walled, dark-brown, divided cells called sclerotic or muriform bodies, which resist killing by neutrophils and macrophages. Melanin in the cell wall protects the fungus. The host responds with a mixed suppurative and granulomatous reaction and marked epidermal thickening (pseudoepitheliomatous hyperplasia), producing the warty surface. Spread is by contiguity, scratching (autoinoculation) and lymphatics; invasion of bone or internal organs is very rare.
Classification
- Nodular: soft pink to violet nodules
- Tumoral: cauliflower-like masses
- Verrucous: dry, warty, hyperkeratotic plaques
- Plaque: scaly, infiltrated plaques
- Cicatricial: plaques with central scarring and active edges; by extent, mild, moderate or severe
Symptoms and signs
- A small painless papule at the site of an old injury, usually on the foot, ankle or leg
- Slow growth over months to years into warty nodules or plaques, often with satellite lesions
- Itching, which spreads lesions by scratching
- Small black dots on the surface (transepidermal elimination of fungus)
- Swelling of the limb in long-standing disease
Diagnosis
- Clinical
- Suspected in a rural worker with a slowly growing warty plaque on a limb; the black dots on the surface are the best spots to sample.
- Tests
- Direct microscopy of scrapings with potassium hydroxide shows the brown sclerotic (muriform) bodies, which confirm the diagnosis. Biopsy shows them inside granulomas with pseudoepitheliomatous hyperplasia; culture on Sabouraud agar grows dark olive-black colonies to identify the species; molecular tests in reference laboratories.
- Imaging
- Usually not needed; ultrasound or MRI can define depth in large lesions, and X-ray is used if bone involvement is suspected.
Differential diagnosis
- Sporotrichosis and other subcutaneous mycoses
- Mycetoma
- Cutaneous tuberculosis (verrucous form) and leprosy
- Cutaneous leishmaniasis
- Squamous cell carcinoma and psoriasis
Goal of treatment
Eliminate the fungus and the lesions, prevent spread and disability, and detect malignant change early; small lesions have the best chance of cure.
Treatment
- Medical
- Long courses of oral antifungals, usually itraconazole or terbinafine, sometimes combined, for many months until clinical and mycological cure.
- Surgical
- Complete surgical excision with a margin for small, early lesions, usually combined with antifungal treatment to avoid relapse.
- Procedure
- Cryotherapy, local heat or laser for limited lesions, combined with drugs in larger ones.
- Follow-up
- Repeat microscopy to confirm mycological cure, monitoring of liver function during long antifungal therapy, and long-term follow-up for relapse and cancer.
Complications
- Bacterial superinfection
- Chronic lymphedema and elephantiasis of the limb
- Squamous cell carcinoma in long-standing lesions
- Scarring, contractures and disability
- Frequent relapse
Prognosis
Early, small lesions are often cured; extensive chronic disease responds slowly, relapses often and leaves disability. It is rarely fatal.
Prevention
- Wearing shoes, gloves and long trousers during farm and forest work
- Cleaning and caring for small skin wounds
- Early consultation for any slowly growing skin lesion
Test yourself
Think of the answer, then tap the question to see it.
How is chromoblastomycosis acquired?
By traumatic implantation of dark-pigmented soil fungi through a thorn, splinter or plant material.
What finding confirms the diagnosis on microscopy?
Thick-walled brown sclerotic (muriform) bodies, the «copper pennies».
Which species is the most common cause in humid Latin America?
Fonsecaea pedrosoi.
Which malignancy can develop in long-standing lesions?
Squamous cell carcinoma.
Related conditions
- Sporotrichosis and other subcutaneous mycoses
- Mycetoma (actinomycetoma and eumycetoma)
- Leishmaniasis
- Cutaneous squamous cell carcinoma
- Lymphoedema
- Leprosy (Hansen disease)
- Paracoccidioidomycosis
- Tuberculosis
- Cellulitis of the leg
- Yaws and endemic treponematoses
Educational information, not medical advice. For any symptom, see a health professional.
Sources: Chromoblastomycosis (DermNet, 2024).
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