Deep Fungal Infections
Superficial mycoses affect only the stratum corneum or mucous membranes. Deep mycoses (systemic and subcutaneous mycoses), by contrast, are a group of diseases in which fungi pass through the epidermis to invade the dermis, subcutaneous tissue, fascia, muscle or bone, or spread through the bloodstream to internal organs.
They fall into two broad groups according to how the fungus enters the body:
- Subcutaneous mycoses: the fungus is introduced directly through a small wound, a thorn prick or a foreign body lodged in the skin.
- Systemic and opportunistic deep mycoses: the fungus enters through the airways (inhaled spores) or the bloodstream and later produces secondary skin lesions, particularly in immunocompromised patients.
At Haute-Derma, deep fungal infections are among the most challenging conditions we see, because the lesions are easily mistaken for cutaneous tuberculosis, nontuberculous mycobacterial (NTM) infection, foreign-body granuloma or squamous cell carcinoma (SCC). Our approach combines histopathology with special stains, direct microscopy and culture, and a coordinated medical and surgical treatment plan.
Pathogenesis and Routes of Infection
Subcutaneous Mycoses
These infections arise when fungal spores from the environment (soil, decaying plant matter, thorns, wood splinters) are implanted directly into the dermis and subcutaneous fat (traumatic inoculation).
- Breach of the skin barrier: once implanted, the fungus adapts to host body temperature (37°C) and begins to change form (from hyphae to yeast or thick-walled cells).
- Suppurative granulomatous reaction: the body responds by recruiting neutrophils that form small abscesses, surrounded by macrophages, epithelioid cells and Langhans giant cells. Long-standing inflammation leads to fibrosis, warty plaques, tissue deformity or draining sinus tracts.
Systemic and Opportunistic Deep Mycoses
- Entry through the lungs: airborne spores are inhaled and cause acute or chronic respiratory infection. From the lungs, the fungus crosses into blood vessels and travels through the circulation to the skin.
- Weakened host immunity: impaired cell-mediated immunity (HIV/AIDS, organ transplantation, long-term systemic corticosteroids, cancer chemotherapy) opens the door for opportunistic fungi to flare up and spread throughout the body.
Our Diagnostic Process at Haute-Derma
Scraping of Black Dots and Direct Microscopy (10–20% KOH):
- Chromoblastomycosis: the black dots on the lesion surface are scraped onto a slide with KOH. Microscopy shows Medlar bodies (muriform cells): round, thick-walled, brick-brown fungal cells divided by internal walls like bricks or coins.
- Cryptococcosis: India ink preparation of lesion fluid shows round yeasts with a wide capsule forming a clear halo around them.
Mandatory Skin Biopsy: a full-thickness biopsy from the dermis down to the subcutaneous fat is taken from the advancing edge of the lesion.
- H&E staining: shows suppurative, necrotizing granulomas containing neutrophils, macrophages and giant cells.
- PAS (periodic acid–Schiff) and GMS (Grocott-Gomori methenamine silver) special stains: always performed to highlight fungal cell walls against the surrounding tissue (magenta with PAS, black with GMS).
Culture and Assessment of Dimorphism: fresh tissue is sent to the microbiology laboratory.
- It is cultured on Sabouraud dextrose agar (SDA) at two temperatures: 25°C (to see the spore-producing mold form) and 37°C (to see the yeast form).
- This confirms the dimorphic nature of organisms such as Sporothrix schenckii or Histoplasma capsulatum.
ITS/18S rRNA Sequencing and Imaging:
- For rare or drug-resistant fungal infections, Haute-Derma arranges PCR and ITS region sequencing to identify the exact species.
- Patients with mycetoma undergo MRI or CT to assess how deeply the infection has invaded the underlying fascia, muscle, bones and joints.
Comprehensive Treatment at Haute-Derma
Deep fungal infections need prolonged treatment that combines systemic medication, surgery when appropriate, and close monitoring of liver and kidney function.
Systemic Antifungal Therapy
- Sporotrichosis:
- First line: itraconazole 200 mg once daily, taken after a fatty meal, for 3–6 months (continuing for at least 2–4 weeks after the skin lesions have fully healed).
- Classic alternative: saturated solution of potassium iodide (SSKI) by mouth, increased gradually from 5 drops three times daily to 30–40 drops three times daily. It works well and is inexpensive but often irritates the stomach and can affect the thyroid.
- Severe or disseminated disease: intravenous liposomal amphotericin B 3–5 mg/kg/day until clinical improvement, then step down to itraconazole maintenance.
- Chromoblastomycosis:
- Itraconazole: 200–400 mg/day alone or combined with terbinafine 250–500 mg/day.
- Treatment lasts 6–12 months or longer, because these thick-walled pigmented fungi are very hard to eradicate completely.
- Eumycetoma:
- Itraconazole: 400 mg/day in two divided doses for 6 months before surgery is considered, then continued for 6–12 months after surgery.
- Voriconazole (200 mg twice daily) or posaconazole is used when itraconazole fails.
- Disseminated cutaneous cryptococcosis:
- Induction: liposomal amphotericin B (3–4 mg/kg/day) plus flucytosine (100 mg/kg/day) for 2 weeks.
- Consolidation and maintenance: fluconazole 400 mg/day for 8 weeks, then 200 mg/day for 6–12 months.
Surgical and Physical Adjunctive Treatments
- Wide surgical debridement: used for localized eumycetoma, small chromoblastomycosis plaques or large necrotic abscesses. Surgery quickly reduces the fungal burden and helps oral antifungals penetrate the tissue better.
- Local hyperthermia: heat packs or a local heating device keep the lesion at 42–43°C for 2–3 hours a day. Sporothrix schenckii and some pigmented fungi are very heat-sensitive, and their growth is suppressed at these temperatures.
- Liquid nitrogen cryotherapy: applied every 2–3 weeks together with oral itraconazole, it helps flatten the warty plaques of chromoblastomycosis quickly.
