Candidiasis
Candidiasis is a group of infections of the skin, mucous membranes and internal organs caused by yeasts of the genus Candida. Unlike the superficial filamentous fungi (dermatophytes), Candida is an opportunistic pathogen that normally lives as part of the human microbiome in the gut, mouth and vagina.
Infection develops when the balance tips between the yeast's virulence and the host's immune defenses. The clinical picture varies enormously: from raw, red intertrigo and satellite pustules on the skin, to white pseudomembranous plaques in the mouth or genital area, to invasive, life-threatening disease in immunocompromised patients.
At Haute-Derma, we approach candidiasis from both a microbiological and an immunological perspective. Rather than simply killing the yeast locally, we identify every underlying predisposing factor so we can restore balance to the skin and mucosal ecosystem.
Microbiology and Opportunistic Pathogenesis
Causative Species
- Candida albicans: The leading cause, responsible for 70%–80% of all skin and mucosal Candida infections.
- Non-albicans Candida (NAC) species: These have increased markedly in recent years and include Candida tropicalis, Candida parapsilosis (often linked to nail infections and medical devices), Candida glabrata, Candida krusei and Candida auris. NAC species behave differently and are more often intrinsically resistant to azole antifungals.
Virulence Factors
- Dimorphism: The yeast switches from its single-celled commensal form (blastoconidia) to pseudohyphae and true hyphae, which can penetrate the epidermal barrier.
- Adhesion: Surface proteins of the ALS (agglutinin-like sequence) family let the yeast attach firmly to host cells.
- Secreted enzymes: Secreted aspartyl proteinases (SAPs) break down keratin and collagen, and phospholipases damage cell membranes, provoking intense inflammation.
- Biofilm: The yeast can encase its colonies in an extracellular polymeric substance (EPS) matrix that shields them from immune cells and blocks antifungal penetration.
Predisposing Factors
- Local: Heat and humidity, occluded skin folds, friction, prolonged moisture or sweat, and overuse of antiseptic washes that disturb the skin's natural pH.
- Systemic: Diabetes (high blood sugar increases the adhesion of Candida), prolonged broad-spectrum antibiotics (which wipe out competing bacteria), systemic or topical corticosteroids, pregnancy, and immunosuppression (HIV/AIDS, organ transplantation, chemotherapy).
Clinical Forms of Candidiasis
Candidiasis is divided into three broad groups by anatomic site:
Cutaneous Candidiasis
- Candidal intertrigo: Affects skin folds (under the breasts, groin, armpits, between the buttocks). The patches are beefy red, moist and weeping, with ragged edges, and are usually surrounded by scattered satellite pustules or papules.
- Candidal paronychia and onychomycosis: Common in people whose hands are often in water. The nail folds become red, swollen and sore, the cuticle is lost, and white pus may be expressed. The nail plate becomes deformed and discolored, starting at the base.
- Candidal diaper dermatitis: Bright red involvement of the groin and thighs in infants, spreading beyond the diaper contact area, with satellite pustules.
- Interdigital erosion (erosio interdigitalis blastomycetica): Usually between the third and fourth fingers; the skin is white, soggy and cracked on a bright red base.
Mucosal Candidiasis
- Oral candidiasis (thrush):
- Acute pseudomembranous form: Curd-like white plaques on the inner cheeks and tongue that leave a raw, bleeding surface when scraped off.
- Erythematous (atrophic) form: Red, burning mucosa, often after antibiotics or inhaled corticosteroids.
- Angular cheilitis: Cracking, red erosions and crusting at both corners of the mouth.
- Vulvovaginal candidiasis (VVC): Intense itching, genital soreness and burning, and a thick, white, clumpy discharge resembling cottage cheese.
- Candidal balanitis: Red patches, small pustules, and itching or burning of the glans and foreskin.
Invasive and Systemic Candidiasis
This includes bloodstream infection (candidemia), endocarditis, retinitis, and deep organ involvement in intensive care (ICU) patients. These forms require transfer to a specialist critical care unit for inpatient treatment.
Differential Diagnosis
| Cutaneous Candidiasis | Dermatophytosis | Erythrasma (Bacterial Intertrigo) |
|---|---|---|
| Opportunistic commensal yeast (Candida spp.) | Keratinophilic filamentous fungi (Trichophyton, Microsporum) | Corynebacterium minutissimum bacteria |
| Bright red, weeping, with surrounding satellite lesions | Red patches with an advancing border and a clearing center | Red-brown or pale pink patches, dry surface, fine scale |
| Moist skin, folds, mucosa, around the nails | Glabrous skin, groin, feet, hands, scalp (mucosa very rarely affected) | Large skin folds (especially groin and armpits) |
| 20% KOH mount: budding yeast cells and pseudohyphae | 20% KOH mount: branching, septate true hyphae | Negative for fungi |
| Wood's lamp: negative | Negative (except some Microsporum species) | Coral-red fluorescence |
Our Diagnostic Workup at Haute-Derma
Digital Dermoscopy:
- Skin and folds: A bright red, weeping background, a thin inward-facing collarette of scale, and prominent satellite pustules with a red halo.
- Around the nails: Loss of the cuticle, dilated capillaries in the nail fold, and a cloudy gray nail plate with redness starting at the base.
Direct Microscopy with 10–20% KOH and Calcofluor White:
- Samples are taken by scraping scale from the edge of the lesion, sampling satellite pustules, or scraping mucosal pseudomembranes.
- Fluorescence microscopy shows clusters of budding yeast cells (blastoconidia) measuring 2–6 µm together with elongated pseudohyphae.
Wood's Lamp Examination: Shining the lamp directly on lesions in the folds quickly rules out erythrasma (coral-red fluorescence) or Pseudomonas infection (green fluorescence).
Chromogenic Agar Culture (CHROMagar Candida): Allows rapid isolation and identification of Candida species by colony color (green: C. albicans; blue: C. tropicalis; pale pink: C. krusei). Antifungal susceptibility testing is performed when treatment fails or azole resistance is suspected.
Comprehensive Treatment at Haute-Derma
Topical Therapy
For mild to moderate infection of the skin, skin folds or mucosa:
- Drying and barrier agents (for weeping intertrigo): Castellani's paint, zinc oxide paste or medical-grade talc applied to the folds twice daily to reduce friction and absorb moisture.
- Polyene and azole antifungals:
- Nystatin cream or pessaries (highly active against Candida).
- Clotrimazole 1%, miconazole 2%, ketoconazole 2%, econazole 1% or sertaconazole 2% cream, applied twice daily for 2–3 weeks.
- Ciclopirox 8% or amorolfine 5% nail lacquer for mild nail involvement.
Systemic Therapy
For extensive infection, persistent mucosal disease, severe paronychia, or patients with underlying conditions (diabetes, immunosuppression):
- Fluconazole (first choice):
- Cutaneous candidiasis / intertrigo / paronychia: 150 mg once weekly (or 50 mg daily) for 2–4 weeks.
- Oral candidiasis: 100–200 mg daily for 7–14 days.
- Vulvovaginal candidiasis: a single 150 mg dose (repeated after 72 hours in severe cases).
- Itraconazole: 200 mg daily for 1–2 weeks (or pulse dosing of 400 mg daily for 1 week each month for nail infection).
- Echinocandins (caspofungin / micafungin): Given intravenously for azole-resistant NAC infections or invasive disease.
Addressing Root Causes and Rebuilding the Skin Barrier
- Managing underlying disease: Working with the patient's physicians to keep blood sugar stable (HbA1c < 7.0%) in diabetes.
- Changing habits: Keep skin folds dry, wear cotton-lined gloves for wet work, and avoid highly alkaline intimate washes.
- Probiotics: Beneficial bacteria (Lactobacillus spp.) help rebalance the microbiome and restore the natural acidic pH of the mucosa.