Chromoblastomycosis

Microbiology and Pathogenesis

Causative Organisms

The disease is caused by brown-to-black pigmented molds found in the environment. The two most common are:

• Fonsecaea pedrosoi: the leading cause in humid tropical climates.
• Cladophialophora carrionii: more common in semi-arid regions.
• Less common species: Phialophora verrucosa, Rhinocladiella aquaspersa and Fonsecaea monophora.

Tissue Transformation and the Formation of Medlar Bodies

• Traumatic inoculation: Fungal spores from soil, tree bark, palm thorns or wood splinters enter the dermis through small scratches in the skin, usually on the lower legs, feet or hands.
• Formation of Medlar bodies (muriform cells): Once inside human tissue, under the pressure of body temperature and the host immune response, the fungus does not grow as hyphae. It converts into very thick-walled, deep reddish-brown spherical structures 5–12 µm across that resemble "copper pennies."
• Reproduction by internal division (fission): Medlar bodies do not bud like ordinary yeasts. They divide by forming internal septa in both horizontal and vertical planes.
• Transepidermal elimination: The body tries to push fungal elements and dead white blood cells out through the skin surface, producing the characteristic tiny black dots on the lesion. These dots are the most valuable spots for microbiological diagnosis.

Main Clinical Forms

• Verrucous form (most common): Hyperkeratotic, warty plaques with a rough, fissured surface resembling a large wart or cauliflower, covered with dry crusts and tiny black dots. They bleed easily with minor trauma.
• Plaque form: Firm, well-demarcated red plaques, slightly raised above the skin, sometimes with fine scale or a small papular rim at the advancing edge. They often heal in the center, leaving atrophic scarring.
• Nodular form: Dark red or light purple nodules with a smooth or slightly uneven surface. They feel firm and slowly enlarge over time.
• Tumorous form: Lesions grow into large, cyst-like masses with an irregular, necrotic, warty surface. Secondary bacterial infection is common, causing a strong odor and pus.
• Cicatricial form: Extensive lesions leave persistent areas of hard, atrophic scarring that can restrict joint movement and seriously deform the limb.

Clinical and Histopathologic Differential Diagnosis

Our Diagnostic Workup at Haute-Derma

Direct Microscopy: the key to a rapid diagnosis

• Sampling technique: A scalpel blade is used to gently scrape the tiny black dots on the surface of the warty lesion, or scale from the lesion's edge.
• Sample preparation: 10–20% KOH solution is added and the slide is gently warmed.
• Findings: Medlar bodies (muriform cells, "copper pennies") seen singly or in clusters: round to oval, very thick-walled, naturally dark brown, with clearly visible internal septa.

Skin Biopsy (Histopathology):

• Epidermis: marked pseudoepitheliomatous hyperplasia with transepidermal elimination.
• Dermis: mixed suppurative granulomatous inflammation. Naturally brown Medlar bodies are seen inside macrophages and Langhans multinucleated giant cells, or lying free in small abscesses. Special stains are usually unnecessary because the fungal melanin is already brown.

Fungal Culture for Species Identification:

• Tissue or skin scrapings are cultured on Sabouraud dextrose agar (SDA) containing chloramphenicol and cycloheximide and incubated at 25–30°C.
• Colonies grow very slowly (2–4 weeks) and are dark olive green, grayish black or velvety black. Microscopy then distinguishes F. pedrosoi (Cladosporium-type branching) from C. carrionii.

Multimodal Treatment at Haute-Derma

Because Medlar bodies have very thick walls and a high melanin content that shields them from the immune system's oxidative attack, single-drug treatment often fails. At Haute-Derma, we combine several approaches:

Systemic Antifungal Therapy

• Itraconazole (standard therapy):
  • Dose: 200–400 mg/day, taken in 1–2 doses right after a main meal.
  • Duration: continuous treatment for 6–12 months, or until the lesions have fully cleared and two consecutive KOH preparations or cultures are negative.
• Terbinafine:
  • Dose: 200–500 mg/day. Particularly effective in combination with itraconazole for treatment-resistant cases.
• Synergistic combination (double antifungal therapy):
  • Used for extensive, long-standing disease: itraconazole 200 mg/day plus terbinafine 250 mg/day. The two drugs block different steps of the fungal ergosterol synthesis pathway.

Physical and Surgical Adjuncts

• Liquid nitrogen cryotherapy:
  • Used for flat plaques, small nodules or the advancing edge of a lesion.
  • Freeze–thaw cycles mechanically break down Medlar body walls and release fungal antigens that stimulate a local immune response.
• Local heat therapy (hyperthermia): daily application of medical-grade heat (42–45°C). Fonsecaea pedrosoi stops growing completely at temperatures above 40°C.
• Local surgical excision: reserved for small (< 3 cm), well-defined lesions. Patients must take itraconazole for at least 2–4 weeks before and after surgery to prevent the fungus from spreading through the bloodstream.