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Candidiasis - A Complete Guide

What Is Candidiasis?

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Pathogenesis & Virulence

• Yeast form - commensal state
• Pseudohyphae - chains of elongated buds
• True hyphae - invasive form, penetrates tissue

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Risk Factors

• Extremes of age (neonates, elderly)
• Diabetes mellitus
• Obesity, pregnancy
• HIV/AIDS
• Broad-spectrum antibiotics, corticosteroids (inhaled or systemic)
• Anti-IL-17 medications (brodalumab, secukinumab, ixekizumab)
• Xerostomia, dentures, radiation to head/neck

• Neutropenia and neutrophil dysfunction
• Hematologic malignancy
• Stem cell or solid organ transplantation
• Indwelling intravascular catheters (central venous lines, hemodialysis)
• ICU admission, abdominal surgery, TPN
• Age >70 years or prematurity in infants

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Classification of Candidiasis

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1. Oropharyngeal Candidiasis (Oral Thrush)

A. Pseudomembranous Candidiasis (Thrush)

• Classic form - white, creamy plaques on erythematous background
• Plaques are removable with a tongue blade, leaving a bleeding surface
• Affects buccal mucosa, palate, tongue, gingiva
• Seen in neonates, immunocompromised patients, those on inhaled steroids

B. Erythematous (Atrophic) Candidiasis

• Shiny, red, depapillated areas of the tongue/palate
• Common under dentures ("denture stomatitis")
• May be the only sign in HIV patients

C. Hyperplastic Candidiasis (Candidal Leukoplakia)

• White plaques that cannot be removed by scraping
• Most often found on the buccal mucosa or tongue
• A premalignant lesion - requires biopsy

D. Angular Cheilitis (Perleche)

• Fissuring, crusting, and erythema at the oral commissures (corners of mouth)
• Often mixed infection with Staphylococcus

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2. Esophageal Candidiasis

• Involves the esophageal mucosa; an AIDS-defining illness
• Symptoms: odynophagia (painful swallowing), dysphagia, retrosternal chest pain
• Endoscopy shows white plaques, erosions, ulcerations
• Most common cause of infectious esophagitis
• Treatment requires systemic azoles (fluconazole 200 mg/day x 14 days) - topical agents do not work here

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3. Cutaneous Candidiasis

A. Candidal Intertrigo

• Affects skin folds: axillae, inframammary, inguinal, perianal, abdominal creases, umbilicus
• Pink-to-red moist patches with a macerated, overhanging epidermal fringe ("collarette scale")
• Key risk: warmth + moisture + occlusion

B. Diaper Dermatitis (Diaper Candidiasis)

• Beefy-red erythematous plaques with satellite papules/pustules in the diaper area
• The satellite pustules beyond the main rash distinguish it from irritant diaper rash

C. Erosio Interdigitalis Blastomycetica

• Macerated whitish plaque on erythematous background in the interdigital webspaces (especially third webspace of hands)
• Seen in chronic wet-work occupations (dishwashers, laundry workers)

D. Candidal Paronychia

• Erythema and swelling of the proximal nailfold with loss of the cuticle
• Can progress to Candidal onychomycosis (5-10% of all onychomycosis)
• More common in fingernails than toenails; associated with pain on pressure

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4. Vulvovaginal Candidiasis (VVC)

• Extremely common; 75% of women have at least one episode
• Symptoms: intense pruritus, burning, thick white "cottage cheese" or curd-like discharge
• Erythema and edema of the vulva; patchy erythema with possible fissures
• Recurrent VVC = 4 or more episodes/year; often requires chronic suppressive therapy

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5. Balanitis / Balanoposthitis

• Candida infection of the glans penis and/or foreskin
• Erythematous plaques with pustules (more common than in vulvitis)
• Often sexually transmitted from a partner with VVC

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6. Candidal Onychomycosis

• Candida invades the nail plate, usually starting from paronychia
• Produces distal subungual infection or total dystrophic onychomycosis
• More common in fingernails than toenails
• Distinctive: painful on pressure (unlike dermatophyte onychomycosis)

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7. Chronic Mucocutaneous Candidiasis (CMC)

• A group of heterogeneous disorders characterized by persistent or recurring Candida infection limited to mucosal surfaces, skin, and nails
• Associated with underlying immune defects - classically a T-cell defect against Candida
• Onset usually in childhood
• Skin involvement can mimic psoriasis (erythematous plaques with scale)
• Associated with AIRE gene mutations (autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy, APECED)
• Requires lifelong suppressive therapy with oral azoles

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8. Invasive Candidiasis / Candidemia

A. Candidemia (Bloodstream Infection)

• Candida detected in blood cultures
• ALL positive blood cultures must be treated (even a single positive bottle), because of the high rate of metastatic seeding to organs
• Classic skin lesion clue: discrete erythematous papules with central pallor or necrosis on trunk/proximal extremities (seen in 10-30% of cases; most common with C. tropicalis)

B. Chronic Disseminated Candidiasis (Hepatosplenic Candidiasis)

• Occurs in neutropenic patients recovering from chemotherapy
• Candida seeds the liver and spleen during neutropenia; lesions become apparent when WBC recovers
• Imaging (CT/MRI) shows bull's-eye lesions in liver/spleen
• Fever that persists despite antibiotic therapy and rising neutrophil count is the key clue

C. Candida Endocarditis

• Most common in IV drug users, patients with prosthetic valves, or those on prolonged TPN
• Very large vegetations
• Very high mortality; often requires surgery + prolonged antifungal therapy

D. Candida Meningitis

• Rare; mainly in neonates, neurosurgical patients, or severely immunocompromised
• C. albicans most common

E. Candida Urinary Tract Infection

• Candiduria is very common in ICU patients with urinary catheters
• Most often represents colonization; only treat if symptomatic, obstructed, or immunocompromised

F. Candida Osteoarticular Infection

• Includes Candida osteomyelitis, septic arthritis, spondylodiscitis
• Usually hematogenous in origin

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Diagnosis

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Treatment Summary

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Quick Summary Table of Types

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Tinea (Dermatophytosis) - Complete Guide

What Is Tinea?

Most Common Species

• Trichophyton rubrum - most common dermatophyte worldwide; causes chronic infections
• T. tonsurans - #1 cause of tinea capitis in the US/UK
• T. mentagrophytes / T. interdigitale - tinea pedis (vesicular type)
• Microsporum canis - from cats/dogs; tinea capitis in Europe

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Classification by Source (Epidemiologic)

Zoophilic and geophilic species trigger a stronger inflammatory response because the human immune system mounts an aggressive reaction against these "foreign" organisms.

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Pathogenesis

1. Adherence - Arthroconidia (infectious spores) attach to the stratum corneum
2. Invasion - Dermatophytes secrete keratinases to break down keratin and invade the stratum corneum
3. Immune evasion - Mannans in their cell walls suppress the immune response (T. rubrum mannans also reduce epidermal turnover, prolonging infection)
4. Containment - They almost never invade beyond keratinized tissue (cooler surface temperature, serum factors like β-globulins, and host immune response limit spread)

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Types of Tinea

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1. Tinea Capitis (Scalp Ringworm)

Clinical Subtypes:

• Caused by M. audouinii, M. canis, M. ferrugineum
• Round/oval patches of scaling alopecia with gray, broken hairs
• Hairs break just above the scalp, leaving a "gray" appearance
• Wood's lamp: bright green fluorescence (ectothrix species)
• Ectothrix = spores on the OUTSIDE of the hair shaft

• Caused by T. tonsurans, T. violaceum
• Hairs break off at scalp level, leaving behind black dots (broken hair stubs)
• Polygonal-shaped alopecia with finger-like margins
• Wood's lamp: NO fluorescence (endothrix species)
• Endothrix = spores INSIDE the hair shaft

• A boggy, painful, purulent mass studded with broken hairs
• Caused by exaggerated host inflammatory response
• More common with zoophilic species (M. canis, T. verrucosum)
• Associated with posterior cervical lymphadenopathy
• Risk of permanent scarring alopecia if untreated
• Often misdiagnosed as bacterial abscess - incision and drainage worsens it!

• Caused by T. schoenleinii
• Scutula (yellow, cup-shaped crusts) around hair follicles
• Hair does not break; progressive, can cause permanent scarring
• Rare; endemic in parts of Africa and Middle East

• Griseofulvin (microsize 20-25 mg/kg/day x 6-8 weeks) - traditional first-line
• Terbinafine (granule formulation FDA-approved) - preferred for Trichophyton
• Fluconazole or itraconazole as alternatives
• Adjunct: selenium sulfide/ketoconazole shampoo to reduce shedding
• For kerion: add short course oral corticosteroids to reduce inflammation and scarring

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2. Tinea Corporis (Ringworm of the Body)

• Active, scaly, advancing border at the periphery
• Central clearing as the infection progresses outward
• Satellite lesions may be present

• Multiple confluent lesions
• Highly inflammatory bullous form (with zoophilic organisms)
• Tinea incognito: atypical appearance caused by corticosteroid misuse (suppresses inflammation, allows deeper spread)
• Majocchi's granuloma: deep follicular invasion; nodular lesions, especially on legs of women who shave

• Topical azoles (clotrimazole, miconazole, ketoconazole) or terbinafine cream x 2-4 weeks for limited disease
• Oral terbinafine, itraconazole, or griseofulvin for extensive or refractory disease
• Caution: do NOT use topical steroids alone (causes tinea incognito)

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3. Tinea Pedis (Athlete's Foot)

Four Clinical Types:

• Dermatophytosis complex: tinea pedis followed by bacterial invasion (gram-negative bacteria colonize macerated fissured skin)
• Dermatophytid reaction (id reaction): vesicular eruption on hands in response to fungal antigen at distant site
• Cellulitis: tinea pedis is a major risk factor for recurrent lower-leg cellulitis

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4. Tinea Cruris (Jock Itch)

• Sharply marginated, erythematous, scaly plaques with active raised border in groin folds
• Extends to inner thighs but spares the scrotum (unlike Candida which involves the scrotum - key differentiator)
• Pruritic; may have central clearing

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5. Tinea Manuum (Ringworm of the Hand)

• Often unilateral (classic pattern: "two feet, one hand" syndrome - bilateral tinea pedis + one hand involved)
• Presents as diffuse hyperkeratosis, scaling, and fissuring of one palm (mimics eczema)
• Often misdiagnosed as contact dermatitis or psoriasis
• More common in people with tinea pedis and onychomycosis
• Treatment: oral antifungals often required due to thick stratum corneum

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6. Tinea Unguium / Onychomycosis (Nail Ringworm)

• Terbinafine 250 mg/day - 6 weeks (fingernails), 12 weeks (toenails) - highest cure rates
• Itraconazole pulse therapy - 200 mg twice daily x 1 week/month
• Topical ciclopirox lacquer (for mild/superficial disease)
• Note: griseofulvin is FDA-approved but has low cure rates for nails

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7. Tinea Barbae (Barber's Itch)

• Superficial: similar to tinea corporis with annular, scaly plaques
• Deep (sycosis barbae): severe folliculitis with boggy, nodular, kerion-like plaques; associated with pustules, crusting, and broken hairs

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8. Tinea Faciei (Face Ringworm)

• Often misdiagnosed as rosacea, seborrheic dermatitis, or lupus
• Annular scaly plaque, but the ring shape may be less obvious on the face
• Worsened by topical corticosteroids (tinea incognito)
• Treatment: topical azoles or terbinafine; oral if extensive

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9. Tinea (Pityriasis) Versicolor

Note: Despite the name "tinea," this is NOT caused by a dermatophyte. It is included here because it is traditionally taught with the tinea group.

• Oval, fine-scaling macules and patches on the chest, shoulders, and upper back (sebaceous-rich areas)
• Hypopigmented lesions on dark skin (organism produces azelaic acid which inhibits tyrosinase → less melanin)
• Hyperpigmented or pink/red lesions on light skin
• May coalesce into large patches; mildly pruritic
• Does NOT tan in the sun (treated areas remain lighter for months)

• KOH preparation: classic "spaghetti and meatballs" appearance - short curved hyphae + round spores
• Wood's lamp: yellow-green or gold fluorescence

• Topical first-line: selenium sulfide shampoo (2.5%), ketoconazole shampoo 2%, zinc pyrithione, ciclopirox olamine
• Apply from neck to knees, leave 10-15 min, rinse; twice weekly x 2-4 weeks
• Oral: fluconazole 200-300 mg weekly x 2-3 weeks, or itraconazole 200 mg/day x 5-7 days
• Post-treatment: pigmentation changes persist for months even after cure
• Maintenance therapy recommended before summer/humid season to prevent recurrence

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Diagnostic Approach

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Treatment Summary

Key rule: Tinea capitis and tinea barbae always require oral therapy. Topical agents cannot penetrate hair follicles.

Ketoconazole oral tablets are no longer recommended as first-line for any superficial fungal infection due to risk of severe hepatotoxicity.

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Quick Reference: All Tinea Types at a Glance

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