Blastomycosis

Blastomycosis, also known as Gilchrist's disease, is a chronic systemic fungal infection caused by the thermally dimorphic fungus Blastomyces dermatitidis (and the more recently described species Blastomyces gilchristii). The spores live in moist soil and decaying wood along rivers and streams. Once inhaled into the lungs, they transform into invasive yeast cells that can spread through the bloodstream to other organs.

In disseminated disease, the skin is the second most commonly affected organ after the lungs (in 40%–80% of patients). Skin lesions are highly destructive and are easily mistaken for squamous cell carcinoma (SCC) or other deep fungal infections unless the key microscopic clue is recognized: broad-based budding yeast. At Haute-Derma, we diagnose cutaneous blastomycosis by combining rapid microbiology with specialist histopathology.

Dimorphic Microbiology and Invasive Pathogenesis

Thermal Dimorphism

  • Environmental form (25°C): The fungus grows as a white to brown mold, producing small conidia (microconidia) 2–10 µm in diameter that become airborne easily.
  • Tissue form (37°C): In human tissue, the spores become large yeast cells (8–15 µm, some up to 30 µm) with a thick, refractile double-contoured wall. They reproduce by broad-based budding, meaning the connection between mother and daughter cell is very wide, nearly as wide as the daughter cell itself.

Routes of Infection and Spread to the Skin

  • Primary lung infection: Microconidia from the environment are inhaled. In the alveoli, the spores escape killing by macrophages thanks to the WI-1 (BAD-1) glycoprotein in their cell wall, which helps the fungus adhere and convert to the yeast form.
  • Hematogenous dissemination: Yeast cells pass from the lungs into the blood and lymphatics and preferentially settle in the skin, bones, genitourinary tract and central nervous system.
  • Primary cutaneous blastomycosis: Extremely rare, occurring only when the fungus is accidentally inoculated directly into the skin (for example, needlestick injuries, laboratory accidents or autopsy work).

Clinical Forms in the Skin

Verrucous Form, the Most Common (70% of Skin Cases):

  • Lesions start as small red papules or nodules, then spread outward into rough, warty hyperplastic plaques.
  • The border is violaceous and sharply raised, studded with tiny purple microabscesses. The surface is covered by dry crust, bleeds easily and heals with central atrophic scarring.

Ulcerative Form: Deep nodules break down into shallow or deep ulcers. The base contains bright red, friable granulation tissue covered with gray necrotic pus. The edges are raised and dark purple, with many small abscesses around the rim.

Subcutaneous Nodular / Abscess Form: Cold abscesses appear that are slightly mobile or fixed to deeper tissue, firm or fluctuant, and eventually open into chronically draining sinus tracts.

Clinical and Histopathological Differential Diagnosis

Blastomycosis (B. dermatitidis)Cutaneous Squamous Cell Carcinoma (SCC)Chromoblastomycosis
Exposure to moist soil or woodland; history of cough/feverSun exposure, old scars, toxinsWood splinter injuries, farm work
Warty or ulcerated plaque with a rim of tiny purple abscessesHard growth with a rough central ulcer and firm rolled edgeWarty plaque with tiny black dots
Large, double-walled yeast with BROAD-BASED buddingNo organismsBrown Medlar bodies (copper pennies)
Pseudoepitheliomatous hyperplasia, suppurative granulomas, broad-based budding yeastAtypical keratinocytes invading through the basement membraneSuppurative granulomas, thick-walled brown Medlar bodies
Responds well to antifungals (itraconazole)Surgical excision / radiotherapyItraconazole + terbinafine + cryotherapy

Our Medical Diagnostic Process at Haute-Derma

Direct Microscopy

  • Technique: Pus is aspirated with a fine needle from the small abscesses at the lesion edge, or the ulcer base is swabbed, and the sample is treated with 10%–20% KOH.
  • Findings: Large spherical yeast cells (8–15 µm) with a thick, refractile double wall. The decisive feature is a single broad-based bud, with a very wide junction between mother and daughter cells.

Essential Skin Biopsy:

  • Epidermis: Marked pseudoepitheliomatous hyperplasia, which is why a biopsy is so easily misread as squamous cell carcinoma if the fungus in the dermis is missed.
  • Dermis: Mixed suppurative granulomatous inflammation with many neutrophils and macrophages.
  • GMS and PAS stains: Highlight the yeast cell walls in black or deep magenta, inside macrophages or free within microabscesses.

Culture and Safe Specimen Handling: Specimens are cultured on Sabouraud dextrose agar (SDA) at 25°C and 37°C. Because the mold form readily releases spores that can infect laboratory staff, cultures must be handled under biosafety level 3 (BSL-3) conditions.

Treatment Protocol at Haute-Derma

Treatment depends on how severe the skin disease is and whether internal organs are also involved:

Mild-to-Moderate Cutaneous Blastomycosis

  • Itraconazole (first-line drug):
    • Dose: 200 mg/day (may be increased to 200 mg twice daily if lesions have not fully responded), taken right after a main meal containing fat.
    • Duration: continued for 6–12 months to prevent relapse or a flare of hidden systemic disease.

Severe or Disseminated Disease

  • Induction phase: Intravenous liposomal amphotericin B (3–5 mg/kg/day) for 1–2 weeks until clear clinical improvement.
  • Consolidation (step-down) phase: Switch to itraconazole 200 mg twice daily for at least 12 months.

Frequently Asked Questions (FAQs)

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